People with a high conspiracy mentality tend to have relatively negative self-views; we don't know the causal link and maximum effect magnitude

Stasielowicz, Lukasz. 2022. “Core Self-evaluations and Conspiracy Mentality.” PsyArXiv. August 5. doi:10.31234/osf.io/sznc9

Abstract: There is mixed evidence of the relationship between conspiracy beliefs and self-appraisal constructs (self-esteem, self-efficacy, or neuroticism). However, in personality research, examining common elements of the three personality traits can be more useful than investigating traits separately. Therefore, the present study examined the relationship between core self-evaluations (CSE) and conspiracy mentality. Based on data of 596 participants, a small negative correlation was found using structural equation modeling (r = -.13, CR 95% [-.22, -.04]). People with a high conspiracy mentality tend to have relatively negative self-views. Future longitudinal studies could help clarify the causal link and maximum effect magnitude. 

Rise and Fall of Empires in the Industrial Era: A Story of Shifting Comparative Advantages

Rise and Fall of Empires in the Industrial Era: A Story of Shifting Comparative Advantages. Roberto Bonfatti & Kerem Coşar. NBER Working Papers 30295. July 2022. DOI 10.3386/w30295

Abstract: The last two centuries witnessed the rise and fall of empires. We construct a model which rationalises this in terms of the changing trade gains from empires. In the model, empires are arrangements that reduce trade cost between an industrial metropole and the agricultural periphery. During early industrialisation, the value of such bilateral trade increases, and so does the value of empires. As industrialisation diffuses, and as manufactures become more differentiated, trade becomes more multilateral and intra-industry, reducing the value of empires. Our results are consistent with long-term changes in income distribution and trade patterns, and with previous historical arguments.

IV Conclusions

“The Foreign and Colonial Offices are chiefly engaged in finding new markets and in defending old ones... Therefore, it is not too much to say that commerce is the greatest of all political interests, and that Government deserves most the popular approval which does the most to increase our trade and to settle it on a firm foundation.” (Joseph Chamberlain talking to the Birmingham Chamber of Commerce in 1896; cited by Ferguson 2004, p. 210)

“[in the mid 1950s] There were signs, particularly through the growth of intraindustry trade and the redirection of overseas investment, that the expansion of the international economy would take place increasingly between advanced economies. [...] Colonial trade, like colonial investment, was becoming less attractive. The pattern of specialisation that had promoted economic integration in the world economy since the nineteenth century was beginning to weaken, and the empires that were its political expression were losing their rationale.” (Hopkins 1997, p. 256).

In this paper, we have added to an otherwise standard trade model “empires” –institutional arrangements that reduce the cost of trading between an industrial center andbthe agricultural periphery. Using this model, we have shown that the emergence and later diffusion of industrialisation, as it occurred in the 19th and 20th century, can explain both the rise and fall of empires in the industrial era. In addition, increasing product differentiation may have further contributed to the demise of empires by incentivising intra-industry trade between developed countries. The above quotes, by prominent British historians, suggest that our model formalises arguments that have been in the historical literature for some time. A similar argument is made for France by Marseille (2015), who posits that French big business evolved from supporting the empire before World War I, to seeing it as a waste of money by the 1950s, largely due to its falling importance in world trade.

We finish with a discussion of how to interpret the model in light of historically relevant factors that we abstracted from. We haven’t allowed for the redistribution of the gains and costs from empire, neither between nor within locations. This suits our current purposes well, since a growing pie will make empires more sustainable, and a shrinking pie less so, however the pie is divided. A richer model, however, would accommodate factors such as coercion through military force, state capacity building and nationalism in the agricultural periphery, and cultural distances across locations. These were important factors in the history of empires. Military force also clearly evolved with industrialisation, since 19th century industrial products such as the Maxim gun gave the industrial centers a military lead which was perhaps comparable to that enjoyed by the first conquistadores in the 16th century.

Finally, the combined assumptions of imperfect specialisation, a spacious world, and lack of discriminatory trade policies against non-empire countries, shut off all strategic interactions amongst the industrial centers. If any of these assumptions is dropped, then to enlarge one’s empire will improve an industrial center’s terms of trade, to the detriment of all the others. This is the context in which competition amongst the industrial centers—such as the Scramble for Africa—could be studied.

Surveys: Continued coral recovery leads to 36-year highs across two-thirds of the Great Barrier Reef, but nothing is said of the average in the whole GBR

Annual Summary Report of Coral Reef Condition 2021/22: Continued coral recovery leads to 36-year highs across two-thirds of the Great Barrier Reef. Australian Institute of Marine Science, no date (YouTube movie dated Aug 3 2022.) https://www.aims.gov.au/monitoring-great-barrier-reef/gbr-condition-summary-2021-22

Summary: In 2022, the [Great Barrier Reef] continues to recover, registering the highest levels of coral cover yet recorded in the Northern and Central regions over the past 36 years (in the Southern part, recovery continued but hard coral cover declined slightly due predator's activity).

[...]

The recovery [...] continues to be driven by [vulnerable corals]. The [Barrier] remains exposed to the predicted consequencies of climate change. [...]. Any future disturbances can rapidly reverse the observed recovery.

Some comments:

1 you won't see the recovery in the news;

2 the AIMS doesn't publish _average_ coral cover since 2017, it only publishes data per region/area (Northern, Central, Southern Barrier);

3 the data above, if aggregated, would show record levels of coral cover since monitoring started for the whole, so, IMHO, it is misleading to say there is recovery in "two thirds of the Great Barrier Reef";

4 we are only monitoring the GBR since the mid-1980s, we don't know how were things before.

Now, why would the AIMS not publish aggregate cover since 2017? Critics think this may be due to a deliberate strategy of making things look worse than they are. Why would they do such a thing? Because of a linear combination of: they are true believers in the superior rights of Nature over us humans; they live off this (the taxpayer finances the surveys, the AIMS and several research positions at universities); the intimate satisfaction of being applauded by important bien-pensants; in a small number of persons, corruption; being good members of the herd; other reasons you may add.

I wrote to the AIMS asking them:

hi, thanks for your work. I got some questions about the reports on the Great Barrier Reef, like https://www.aims.gov.au/monitoring-great-barrier-reef/gbr-condition-summary-2021-22...:

1   what was the motivation to stop considering relevant the coral cover average, across all regions, which is no longer published (since, at least, 2017, as seen in "The whole GBR," https://www.aims.gov.au/reef-monitoring/gbr-condition-summary-2016-2017)?

2  are there papers in scientific publications about how good would it be to abandon publishing the cover average?;

3  does anyone knows what would be the result if the average were computed?; and

4  do they plan to start publishing again the average?

Once they reply I will post here their answer.

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Update Jul 31 2023: no reply until now

Across the first two decades of the 2000s, there is an increasing disinterest in becoming fathers among childless men

An increasing disinterest in fatherhood among childless men in the United States: A brief report. Robert Bozick. Journal of Marriage and Family, July 30 2022. https://doi.org/10.1111/jomf.12874

Abstract

Objective: The goal of this brief report is to document trends in expectations for and attitudes toward fatherhood among childless men across the first two decades of the 2000s.

Background: Childless men account for more than a third of adult men in the United States, but it is unclear if they desire to become fathers, and if not, whether this sentiment changed over time.

Method: Time trends for multiple measures of expectations for and attitudes toward fatherhood are plotted using samples of childless men from the National Survey of Family Growth, the Monitoring the Future study, and the Panel Study of Income Dynamics' Transition to Adulthood supplement.

Results: Across the time series, a growing share of childless men do not want children and increasingly, a lack of children would not bother them at all. Additionally, certainty in having children among childless men has waned over time and fewer childless men are concerned with parental leave policies when evaluating their job options.

Conclusion: Across the first two decades of the 2000s, there is an increasing disinterest in becoming fathers among childless men. These trends have broad implications for family researchers who study fertility rates, men's health, and family relationships.

Collective mental time travel: People have a more negative perception of the collective future than the personal future, maybe due to the press magnifying negative views

Collective mental time travel: Current research and future directions. Meymune N. Topcu, William Hirst. Progress in Brain Research, August 4 2022. https://doi.org/10.1016/bs.pbr.2022.06.002

Abstract: In this chapter, we will provide a review on the emerging psychological literature on collective mental time travel (MTT). Our review will focus on the cognitive aspects of remembering the collective past and imagining the collective future. We will explore factors such as specificity, phenomenal characteristics, content, and valence. We will also include brief overviews of cultural and social psychological research that is relevant to the topic of collective MTT. In these overviews, we will examine the research on narratives, collective continuity, collective angst, and human action. Three main themes will emerge from these discussions: the connection between collective past and future thinking, the differences between collective past and future thinking, and the role of goals, perceived agency, and collective action. We will integrate the findings of cognitive, cultural, and social psychological work through these three themes and offer ways to move collective MTT research forward.

Keywords: Collective memoryCollective future thinkingMental time travelValencePerceived agencyGoalsNarrativesCollective continuityCollective action

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people have a more negative perception of the collective future than the personal, maybe due to the press magnifying negative views

Check also: Topcu, M. N., & Hirst, W. (2020). Remembering a nation’s past to imagine its future: The role of event specificity, phenomenology, valence, and perceived agency. Journal of Experimental Psychology: Learning, Memory, and Cognition, 46(3), 563–579. https://doi.org/10.1037/xlm0000746

Abstract: People are routinely involved in remembering the national past and imagining the national future, especially when making political decisions. These processes, however, have not been explored extensively. The present research aims to address this lacuna. In 2 experiments (N = 203), participants were asked to remember and imagine events that involve the United States. Later, they rated these events in terms of phenomenal characteristics, valence, and perceived agency (circumstance, self, other-people, nation). Their responses were also coded for specificity and content. Past and future responses correlated for specificity, phenomenology, valence, and the four domains of perceived agency. Despite this strong correspondence between past and future thinking, there were also differences. Future responses were less specific and more positive than past responses. Moreover, people thought that they themselves and their nation will have more control over their nation’s future compared with the control they attributed to themselves and their nation over its past. The bias to be more optimistic about the nation’s future was partly explained by this tendency to see the nation as more agentic in the future. Taken together, these results reveal striking similarities and divergences between autobiographical and collective mental time travel. The present research provides an exploration for the newly emerging field of collective mental time travel. 

Why is exposure to opposing views aversive? Reconciling three theoretical perspectives.

Why is exposure to opposing views aversive? Reconciling three theoretical perspectives. Julia A. Minson, Charles A. Dorison. Current Opinion in Psychology, August 4 2022, 101435. https://doi.org/10.1016/j.copsyc.2022.101435

Abstract: To form truthful beliefs, individuals must expose themselves to varied viewpoints. And yet, people routinely avoid information that contradicts their prior beliefs—a tendency termed “selective exposure.” Why? Prior research theorizes that that exposure to opposing views triggers negative emotions; in turn, people avoid doing so. Here, we argue that understanding why individuals find simple exposure to opposing perspectives aversive is an important and largely unanswered psychological question. We review three streams of research that offer relevant theories: self-threat borne of cognitive dissonance; naïve realism (i.e., the illusion of personal objectivity); and reluctance to expend cognitive effort. While extant empirical research offers the strongest evidence for predictions from naïve realism, more systematic research is needed to reconcile these perspectives.

Environmental factors play a greater role in the etiology of psychotic experiences than genetic factors: some groups of individuals with seemingly low genetic risk for psychotic experience may develop them if exposed to high levels of environmental risk

Taylor MJ, Freeman D, Lundström S, Larsson H, Ronald A. Heritability of Psychotic Experiences in Adolescents and Interaction With Environmental Risk. JAMA Psychiatry. Published online August 03, 2022. doi:10.1001/jamapsychiatry.2022.1947

Key Points

Question  Are psychotic experiences less heritable for adolescents who experience more environmental risk factors?

Findings  In a twin study of 4855 twin pairs aged 16 years from the UK, the relative importance of genetic influences on certain psychotic experiences diminished with more exposure to environmental risk factors. A similar pattern of results was observed in an independent sample from Sweden (N = 8568 pairs).

Meaning  These results suggest gene-by-environment interactions in relation to psychotic experiences; some groups of individuals with seemingly low genetic risk for psychotic experience may develop them if exposed to high levels of environmental risk, in a similar manner to clinical observations in relation to schizophrenia.

Abstract

Importance  Genetic risk factors are known to play a role in the etiology of psychotic experiences in the general population. Little is known about whether these risk factors interact with environmental risks for psychotic experiences.

Objective  To assess etiological heterogeneity and exposure to environmental risks associated with psychotic experiences in adolescence using the twin design.

Design, Setting, and Participants  This twin study, conducted from December 1, 2014, to August 31, 2020, included a UK-based sample of twin pairs aged 16 years. This investigation evaluated the extent to which the genetic variance underlying psychotic experiences and the magnitude of the heritability of psychotic experiences was moderated by exposure to 5 environmental risk factors (bullying, dependent life events, cannabis use, tobacco use, and low birth weight). Psychotic experiences were assessed by 5 self-reported measures and 1 parent-reported measure. Participants’ exposure to environmental risks was assessed at birth and age 12 to 16 years. Structural equation models were used to assess differences in the variance in and heritability of psychotic experiences across these exposures, while controlling for gene-environment correlation effects. Analyses were repeated in an independent Swedish sample. Data analyses were performed from September 1, 2018, to August 31, 2020.

Main Outcomes and Measures  Primary outcome measures were exposure to environmental factors, as measured by a composite score, and psychotic experiences.

Results  A total of 4855 twin pairs (1926 female same-sex pairs, 1397 male same-sex pairs, and 1532 opposite-sex pairs) were included from the Twins Early Development Study (TEDS), and 6435 twin pairs (2358 female same-sex pairs, 1861 male same-sex pairs, and 2216 opposite-sex pairs) were included from the Child and Adolescent Twin Study in Sweden (CATSS). Mean age of twins from TEDS was 16.5 years. Mean age of twins from CATSS was 18.6 years. More exposure to environmental risk factors was associated with having more psychotic experiences. The relative contribution of genetic influences to psychotic experiences was lower with increasing environmental exposure for paranoia (44%; 95% CI, 33%-53% to 38%; 95% CI, 14%-58%), cognitive disorganization (47%; 95% CI, 38%-51% to 32%; 95% CI, 11%-45%), grandiosity (41%; 95% CI, 29%-52% to 32%; 95% CI, 9%-48%), and anhedonia (49%; 95% CI, 42%-53% to 37%; 95% CI, 15%-54%). This pattern was replicated for the measure of psychotic experiences in the independent Swedish replication sample. The heritability of hallucinations and parent-rated negative symptoms remained relatively constant.

Conclusions and Relevance  Findings of this twin study suggest that environmental factors play a greater role in the etiology of psychotic experiences than genetic factors. The relative importance of environmental factors is even higher among individuals exposed to environmental risks for psychotic experiences, highlighting the importance of a diathesis-stress or bioecological framework for understanding adolescent psychotic experiences.

Discussion

In this cohort study, we tested whether the heritability of adolescent psychotic experiences changes with exposure to environmental risks associated with psychotic experiences. Results suggest a gene-by-environment interaction for paranoia, hallucinations, cognitive disorganization, grandiosity, and anhedonia. The findings were replicated in an independent Swedish sample, thus lending robustness to our results. Our study thus suggests differences in heritability of certain psychotic experiences that may be associated with environmental exposures.

Specifically, there was an observed reduction in heritability of psychotic experiences in the presence of environmental exposures. These results are consistent with a bioecological framework, which would predict that more favorable environments would lead to higher heritability.²⁰Our results run contrary to a diathesis-stress pathway to psychotic experiences, which would predict that environmental risks trigger a genetic susceptibility to a given disorder and would thus lead to higher heritability of a phenotype in the presence of environmental risks.²⁰

It is also important to put our results in the context of prior studies of gene-by-environment interaction in relation to psychotic experiences. One study³³ reported that the association between environmental risks and psychotic experiences increased among individuals with a family history of psychosis. Although this finding also supports gene-by-environment interaction, the results are somewhat different than what would be expected from our analyses because our analyses suggest that genetic factors were less salient in the presence of environmental exposures. Moreover, other studies^34,35 have found no evidence of gene-by-environment interaction for psychotic experiences. Methodological differences may underlie these discrepancies. First, family history is not the same as genetic influence because family history includes a combination of genetic and shared environmental factors. Second, we focused on a composite exposure score comprising 5 environmental factors; prior studies have focused on more specific factors, including childhood physical abuse³⁵ and trauma.³⁴ Third, we focused on 6 specific psychotic experiences here, whereas prior studies used single measures. Finally, it is important to note that prior studies focus specifically on the interaction between genetic risk for psychotic experiences based on family history, by contrast with the current study that used the twin design. In our study, we tested whether heritability differed dependent on exposure to environmental risks. Heritability is a population statistic, and as such, an approach based on calculating heritability is somewhat different from an approach based on using family history as a proxy for individual genetic risk.

On a clinical level, it is first important to clarify that we focused on a young sample, who were aged 16 or 18 years. Many of these individuals will be too young to have been diagnosed with a psychotic disorder, but it is known that psychotic experiences in this age group can lead to severe clinical conditions in some individuals. Nonetheless, clinically it is often noted that many individuals with schizophrenia do not have a family history of schizophrenia. Indeed, although the relative risk for schizophrenia is increased among relatives of individuals diagnosed with schizophrenia, most relatives of individuals with schizophrenia do not develop schizophrenia.³⁶ Our results extend these observations to adolescent psychotic experiences and indicate that they may develop in a variety of contexts. Specifically, our results suggest that psychotic experiences may be prevalent in populations with a high degree of exposure to environmental risks associated with psychotic experiences. Indeed, there is substantial conjecture that psychotic experiences can be reached through multiple pathways, such as pathways that are more based on genetic propensity and others that are more down to environmental risks; however, to our knowledge, this is one of the first studies to provide replicable empirical findings on this topic.

The previously mentioned arguments should be tempered, however, for certain types of psychotic experiences. Although we observed that the heritability differed according to environmental exposure for some psychotic experiences, the heritability was more consistent for hallucinations and negative symptoms. This is important from a clinical perspective, given that negative symptoms are thought to be particularly predictive of subsequent mental illness. As such, these results lend further weight to the argument that the etiology of psychotic experiences may differ according to specific subtypes of psychotic experience.⁸

Strengths and Limitations

Strengths of our study included the use of 2 representative, population-based samples in different countries. In 1 sample, we measured 6 different specific psychotic experiences, enabling us to consider gene-by-environment interactions for different psychotic experiences. There were several limitations, however. Although we employed data from both the UK and Sweden, we still only focused on 2 European countries. Many of our exposures may differ in prevalence across the world, and it would therefore be useful to assess whether similar results emerge in countries with more environmental variability than the UK and Sweden. Our measures of tobacco and cannabis use were more brief than our other measures. Future studies should use more detailed measures. We also created a composite score that involved counting the number of exposures each participant had undergone, which included summing exposures that may have different etiologies or mechanisms underlying their association with psychotic experiences. Further, although our model has controlled for gene environment correlation, we recognize that birth weight is a complex phenotype influenced by parent and child genetics and prenatal environment.

It is further important to be aware that the environmental composite is not identical across TEDS and CATSS. The life events scale, for example, includes items about increasing numbers of quarrels with parents in CATSS, which are not covered in TEDS. Percentile-based cutoffs were used to define low birth weight; birth weight was lower in TEDS than CATSS on average, and therefore, this led to heavier twins being captured in CATSS. Exclusion criteria also differed between samples; individuals with extreme obstetric complications were excluded from TEDS but not CATSS. The fact that we observed similar results between CATSS and TEDS gives us confidence that these differences did not strongly influence our results; however, they should nevertheless be interpreted with these differences in measure in mind. Finally, twins are generally born lighter than singletons. We included birth weight as an exposure here, and hence, individuals with very low birth weight may have been overrepresented in our sample. However, studying birth weight in twins here is unlikely to create any issues for generalizability for 2 reasons. First, our modeling analyses were focused on variance rather than mean differences. Second, twins were compared with twins in the design (not singletons); as such, modest mean differences between singletons and twins in birth weight did not affect the findings.

Widely cited psychology study, suggesting that winners of competitions are more likely to cheat subsequently, fails to replicate

Does competitive winning increase subsequent cheating? Andrew M. Colman, Briony D. Pulford, Caren A. Frosch, Marta Mangiarulo and Jeremy N. V. Miles. Royal Society Open Science, Volume 9, Issue 8, August 3 2022. https://doi.org/10.1098/rsos.202197

Abstract: In this preregistered study, we attempted to replicate and substantially extend a frequently cited experiment by Schurr and Ritov, published in 2016, suggesting that winners of pairwise competitions are more likely than others to steal money in subsequent games of chance against different opponents, possibly because of an enhanced sense of entitlement among competition winners. A replication seemed desirable because of the relevance of the effect to dishonesty in everyday life, the apparent counterintuitivity of the effect, possible problems and anomalies in the original study, and above all the fact that the researchers investigated only one potential explanation for the effect. Our results failed to replicate Schurr and Ritov's basic finding: we found no evidence to support the hypotheses that either winning or losing is associated with subsequent cheating. A second online study also failed to replicate Schurr and Ritov's basic finding. We used structural equation modelling to test four possible explanations for cheating—sense of entitlement, self-confidence, feeling lucky and inequality aversion. Only inequality aversion turned out to be significantly associated with cheating.

3. Discussion

Schurr & Ritov's [1] experiments were severely underpowered and vitiated by other design and methodological problems. In particular, their basic finding that competitive winning is associated with subsequent cheating was based on a study in which participants were not assigned randomly to experimental and control treatment conditions. Our study 1 replicated Schurr and Ritov's study as closely as possible with adequate power and random assignment to experimental and control conditions. We observed significant levels of cheating in both experimental and control conditions but failed to replicate Schurr and Ritov's basic finding of higher cheating by winners, although the experimental manipulation of winning or losing in both of our experiments was identical to Schurr and Ritov's. We also found no evidence for any significant effect of competitive losing on cheating in the subsequent game of chance.

In study 2, we tested the hypotheses that competitive winning or losing is associated with subsequent cheating in an even larger experiment, conducted online, with participants assigned randomly to winning, losing, paired control, and unpaired control treatment conditions. Once again, we observed significant levels of cheating in all treatment conditions but found no evidence to support the hypotheses that either winning or losing is associated with subsequent cheating. There was no significant difference in cheating between our paired and unpaired control conditions—whether cheating was associated with money being taken from another participant or from the experimenter.

This study also included an investigation, using SEM, to test the hypotheses that winning is associated with a latent variable that we labelled 'pride', indicated by self-confidence, a feeling of luckiness, and a sense of entitlement, and that pride is associated with subsequent cheating, or that losing is associated with a latent variable of 'shame', indicated by a sense of entitlement and inequality aversion, and that shame is associated with subsequent cheating. We measured all the indicator variables with psychometric scales that showed high reliability in our study, and the only significant association that emerged was between inequality aversion and cheating. This suggests that participants who were least inequality-averse were most likely to cheat in the coin-flip game, whether they had won or lost the previous competitive perceptual task. The association of inequality aversion with cheating was not strong, but it is worth investigating experimentally. It may reflect a more general sense of fairness among participants who are inequality averse. If those who value fairness strongly tend to be inequality averse and also construe cheating as a form of unfairness, the association would be explained, but that explanation requires further experimental evidence.

One key question that needs to be addressed is why the results of both of our studies failed to replicate Schurr & Ritov's [1] basic finding that competitive winning is associated with subsequent cheating in a game of chance. One possibility is that Schurr and Ritov's finding, based as it was on a severely underpowered study without proper random assignment to experimental and control groups, cannot validly be inferred from their results. A second possibility relates to their unusual methodology, in which half the participants in every testing session were randomly assigned as passive participants, whose only role was to receive the money that the other half—the active participants—left behind after taking what they claimed was owing to them after the dice game. In our studies, the participants were told that the money that they left behind would go to ‘the other person you are paired with’, with the implication that it was one of the other participants, and in that sense, from the participants' point of view, it was similar to what Schurr and Ritov's participants believed. However, the active participants in Schurr and Ritov's experiment believed that the money they left would go to others who had done absolutely nothing in the experiment, whereas the participants in our replications could have believed that the money would go to others who were fully participating. All of Schurr and Ritov's participants who rolled the dice were told that ‘The rest of the money will go to one of the participants sitting in the lab who did not play the two-dice-under-a-cup game’ [1, p. 1757]. This might possibly explain the failure of our experiments to replicate Schurr and Ritov's basic finding if their winners, in contrast to ours, believed that the recipients of money left behind were more deserving of being cheated, but that would suggest that the basic finding applies only in the artificial context of their experimental setup or in very limited and unusual circumstances. In everyday life, people who cheat rarely, if ever, know that their victims have done nothing to earn the money out of which they are being cheated. A third possibility is that the discrepancy between Schurr and Ritov's findings and ours arises from a cross-cultural difference between students in Israel and the UK; but we are unaware of any evidence that might support that interpretation, it is very unlikely given that Israel and the UK are both WEIRD (western, educated, industrialized, rich, democratic) cultures [36], and if correct it would severely limit the generality of Schurr and Ritov's basic finding (and also, by symmetry, our own basic finding).

Given the published evidence that more cheating tends to occur in online than laboratory studies [26,27], it is worth noting that we found no such difference. In study 1, incentives were lower than in study 2 and participants cheated, on average, by 31p out of a possible maximum of £3.00 (10.3%), while in study 2 they cheated by £3.25 out of a maximum of £50.00 (6.5%). The incentives were much greater in study 2, therefore participants' cheating translated into greater monetary terms in study 2. In our laboratory-based study 1, using Cohen's [11] index of effect size, the overall effect size of cheating was d = 0.46 and in our online study 2 it was d = 0.42. The finding of such a negligible difference can perhaps be explained by the fact that the dice-under-a-cup game that we used in the laboratory in study 1 provides an opportunity for cheating that seems almost entirely ‘safe’, in the sense that it would be impossible to detect a particular instance of cheating. If that interpretation is right, then our online experiment, in which the corresponding task was a coin-flip task, may not have provided a significantly greater sense of security, and participants may have felt equally disinhibited from cheating in both experiments. Thus the general cheating that we found across all conditions would be in line with recent evidence that cheating tends to occur particularly when it is unobservable by the experimenters [37].

Our studies have not provided much enlightenment as to what leads some people to cheat. In both studies, cheating occurred at a low but significant level in all treatment conditions, and the only psychometric variable that correlated significantly with cheating was inequality aversion. Our SEM revealed only one path that reached statistical significance, from shame to number of heads claimed and hence cheating. One of the indicators of shame was inequality aversion. Further research is clearly required to determine whether inequality aversion is indeed causally related to cheating and if so why. One possibility is that inequality aversion is associated with a more general concern for fairness and that people who value fairness are less likely to cheat because they perceive cheating as a form of unfairness, but without further evidence this interpretation remains speculative.

The aim of study 2 was to discover variables, possibly but not necessarily including competitive winning or losing, that might explain cheating in a subsequent game of chance. The SEM should reveal whether, and if so how, winning or losing is implicated. We hypothesized that sense of entitlement, self-confidence, personal luckiness and inequality aversion might help to explain cheating. For example, if Schurr & Ritov [1] were right, then winning should be associated with sense of entitlement and sense of entitlement should be associated with cheating. Sense of entitlement is interpreted by the authors of the scale that we used to measure it [31] as a personality trait, and we should perhaps expect a personality trait to be largely unaffected by an experimental manipulation such as winning or losing. However, the SEM does not require winning or losing to play any part in the potential relationship of any of the other variables to cheating. For example, we might have found that trait sense of entitlement is associated with cheating, irrespective of any association with winning or losing, just as we did, in fact, find that inequality aversion is associated with cheating without any significant association with winning or losing.

 

Contra Saez, Piketty et al., in a world in which ideas drive GDP, maximizing the welfare of the middle class and below requires a lower, not higher top tax rate

Taxing Top Incomes in a World of Ideas. Charles I. Jones. Journal of Political Economy, Aug 2022. https://doi.org/10.1086/720394

Abstract: This paper considers top income taxation when (i) new ideas drive economic growth, (ii) the reward for successful innovation is a top income, and (iii) innovation cannot be perfectly targeted by a research subsidy—think about the business methods of Walmart, the creation of Uber, or the “idea” of Amazon. These conditions lead to a new force affecting the optimal top tax rate: by slowing the creation of new ideas that drive aggregate GDP, top income taxation reduces everyone’s income, not just income at the top. This force sharply constrains both revenue-maximizing and welfare-maximizing top tax rates.

Abstract of a 2019 version, which refers to Saez by name: This paper considers the taxation of top incomes when the following conditions apply: (i) new ideas drive economic growth, (ii) the reward for creating a successful innovation is a top income, and (iii) innovation cannot be perfectly targeted by a separate research subsidy --- think about the business methods of Walmart, the creation of Uber, or the "idea" of Amazon.com. These conditions lead to a new force affecting the optimal top tax rate: by slowing the creation of the new ideas that drive aggregate GDP, top income taxation reduces everyone's income, not just the income at the top. When the creation of ideas is the ultimate source of economic growth, this force sharply constrains both revenue-maximizing and welfare-maximizing top tax rates. For example, for extreme parameter values, maximizing the welfare of the middle class requires a negative top tax rate: the higher income that results from the subsidy to innovation more than makes up for the lost redistribution. More generally, the calibrated model suggests that incorporating ideas as a driver of economic growth cuts the optimal top marginal tax rate substantially relative to the basic Saez calculation.

[Some can admit to the unavoidability of going downwards, to a less rich world, if we want to redistribute and have no upper class...: Revolutionaries in societies that used 1/4 as much energy as we do thought communism right around the corner; let's get the abundance that matters (everyone be free to pursue learning, play, sport, amusement, companionship, & travel) https://www.bipartisanalliance.com/2019/05/revolutionaries-in-societies-that-used.html]

1. Introduction

This paper considers the taxation of top incomes when the following conditions apply: (i) new ideas drive economic growth, (ii) the reward for creating a successful new idea is a top income, and (iii) innovation is broad-based and cannot be perfectly targeted by a separate research subsidy.

The classic tradeoff in the optimal taxation literature is between redistribution and the incentive effects that determine the “size of the pie.” But in most of that literature — starting with Mirrlees (1971), Diamond (1998), Saez (2001) and Diamond and Saez (2011) — the “size of the pie” effects are relatively limited. In particular, when a top earner reduces her effort because of a tax, that reduces her income but may have no or only modest effects on the incomes of everyone else in the economy.

In constrast, I embed the optimal tax literature in the idea-based growth theory of Romer (1990), Aghion and Howitt (1992), and Grossman and Helpman (1991). According to this literature, the enormous increase in living standards over the last century is the result of the discovery of new ideas — perhaps by a relatively small number of people. To the extent that top income taxation distorts this innovation, it can impact not only the income of the innovator but also the incomes of everyone else in the economy.

The nonrivalry of ideas is key to this result and illustrates why incorporating physical capital or human capital into the top tax calculation is insufficient. If you add one unit of human capital or one unit of physical capital to an economy — think of adding a computer or an extra year of education for one person — you make one worker more productive, because these goods are rival. But if you add a new idea — think of the computer code for the original spreadsheet or the blueprint for the electric generator — you can make any number of workers more productive. Because ideas are nonrival, each person’s wage is an increasing function of the entire stock of ideas. A distortion that reduces the production of new ideas therefore impacts everyone’s income, not just the income of the inventor herself.

A standard policy implication in this literature is that it may be optimal to subsidize formal R&D, and one could imagine subsidizing research but taxing top incomes as a way to simultaneously achieve both efficient research and socially-desirable redistribution. Instead, we consider a world with both basic and applied research. Basic research uncovers fundamental truths about the way the world works and is readily subsidized with government funding. Applied research then turns these fundamental truths into consumer products or firm-level process innovations. This is the task of entrepreneurs and may not be readily subsidized as formal R&D. Think about the creation of Walmart or Amazon.com, organizational innovations in the health care and education industries, the latest software underlying the Google search engine, or even the creation of nonrival goods like a best-selling novel or the most recent hit song. Formal R&D is a small part of what economists would like to measure as efforts to innovate. For example, around 70% of measured R&D occurs in the manufacturing industry. In 2012, only 18 million workers (out of US employment that exceeds 130 million) were employed by firms that conducted any official R&D. 1 According to their 2018 corporate filings, Walmart and Goldman-Sachs report doing zero R&D.

The idea creation and implementation that occurs beyond formal R&D may be distorted by the tax system. In particular, high incomes are the prize that motivates entrepreneurs to turn a basic research insight that results from formal R&D into a product or process that ultimately benefits consumers. High marginal tax rates reduce this effort and therefore reduce innovation and the incomes of everyone in the economy. Taking this force into account is important quantitatively. For example, consider raising the top marginal tax rate from 50% to 75%. As we discuss below, in the United States, the share of income that this top marginal rate applies to is around 10%, so the change raises about 2.5% of GDP in revenue before the behavioral response. In the baseline calibration, such an increase in the top marginal rate reduces innovation and lowers GDP per person in the long run by around 6 percent. With a utilitarian welfare criterion, this obviously reduces welfare. But even redistributing the 2.5% of GDP to the bottom half of the population would leave them worse off on average: the 6% decline in their incomes is not offset by the 5% increase from redistribution. In other words, unless the social welfare function puts disproportionate weight on the poorest people in society, raising the top marginal rate from 50% to 75% reduces social welfare.

We consider various revenue- and welfare-maximizing top tax rate calculations, first ignoring the effect on innovation and then taking it into account. For a broad range of parameter values, the effects are large. For example, in a baseline calculation, the revenue-maximizing top tax rate that ignores the innovation spillover is 92%. In contrast, the rate that incorporates innovation and maximizes a utilitarian social welfare function is just 22%. Moreover, if ideas play an even more significant role than assumed in this baseline, it is possible for the optimal top income tax rate to turn negative: the increase in everyone’s income associated with subsidizing innovation exceeds the gains associated with redistribution.

Importantly, however, the point of this paper is not to estimate “the” optimal top income tax rate. Such a calculation involves many additional considerations documented in the existing literature (reviewed below) that are omitted from the analysis here. Instead, the point is that future work aimed at calculating such a number will certainly want to explicitly consider the effects of top income taxation on the creation of new ideas. They appear to be quantitatively important.

The remainder of the paper is organized as follows. After a brief literature review, Section 2 lays out the steady-state of a rich dynamic growth model and considers the top tax rate that maximizes revenue, along the lines of Diamond and Saez (2011) and others. Section 3 then considers the tax scheme that maximizes the welfare of the “bottom 90%” or the median voter (they are the same people here). This turns out to matter quantitatively: the planner cares about distorting the creation of ideas not merely because it affects the revenue that can be earned by regular workers, but because it affects their consumption and economic growth directly. This setup is especially convenient for two reasons. First, it yields a nice closed-form solution. Second, it allows us to remain agnostic about the source of the behavioral tax elasticity for top earners: whether this comes from an effort choice or an occupational choice or from something else is irrelevant; we just need to know the elasticity.

Section 4 goes further and finds the tax system that maximizes a utilitarian social welfare function. While this objective function is obviously of interest, the solution does not admit a closed-form expression. In addition, we must be explicit about the nature of the behavioral tax elasticity for top earners, which makes the model less general. Section 5 discusses additional results and extensions, including empirical evidence on growth and top income taxation. Finally, Section 6 builds the full dynamic growth model that nests the simple model as a special case in the steady state. 

Research indicates that people will behave in ways that are consistent with the genes they believe they possess; it is applicable too to the context of risk-taking

Genetic Risk Information Influences Risk-Taking Behavior. Ryan Wheat, Matthew Vess and Patricia Holte. Social Cognition, Vol. 40, No. 4. August 2022. https://doi.org/10.1521/soco.2022.40.4.387

Abstract: Research indicates that people will behave in ways that are consistent with the genes they believe they possess. We examined this tendency in the context of risk-taking. We predicted that bogus genetic testing results indicating a propensity for risk-taking would cause participants to demonstrate riskier behavior. Participants submitted saliva tests and were randomly assigned to receive bogus genetic feedback indicating high propensity or low propensity for risk-taking. They then completed a standardized measure of risk-taking behavior. Results showed that those who received feedback indicating they were genetically disposed to risky behavior demonstrated higher risk-taking behavior than those who received feedback indicating that they were genetically disposed to risk aversion. These findings extend work on genetic feedback effects to a new domain and further reveal the ways that genetic feedback shapes behavior independent of one's actual genetic propensities.

Across both studies, most participants did not try to stop the staged theft or even report it to the experimenter afterward; they predicted much greater intervention in advance

See something, say something? exploring the gap between real and imagined moral courage. Nathan S. Kemper,Dylan S. Campbell &Anna-Kaisa Reiman. Ethics & Behavior, Jul 27 2022. https://www.tandfonline.com/doi/abs/10.1080/10508422.2022.2104282

Abstract: Research shows that people often do not intervene to stop immoral action from happening. However, limited information is available on why people fail to intervene. Two preregistered studies (Ns = 248, 131) explored this gap in the literature by staging a theft in front of participants and immediately interviewing them to inquire about their reasons for intervening or not intervening. Across both studies, most participants did not try to stop the theft or even report it to the experimenter afterward. Furthermore, many participants reported confusion and inattention as precursors to nonintervention, yielding insight into what inhibits moral courage.

Keywords: Moral couragemoral judgmentbehavioral experimentqualitative methods

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We observed substantial overestimation, with participants who imagined witnessing a theft being nearly ten times more likely to say they would intervene, compared to the actual rate of intervention.

Despite the declining quality of income data: While overall income inequality rose over the past five decades, the rise in overall consumption inequality was small

Consumption and Income Inequality in the U.S. Since the 1960s Bruce D. Meyer and James X. Sullivan. Journal of Political Economy, June 28, 2022. https://doi.org/10.1086/721702

Abstract: Recent research concludes that the rise in consumption inequality mirrors, or even exceeds, the rise in income inequality. We revisit this finding, constructing improved measures of consumption, focusing on ints well measured components that are reported at a high and stable rate relative to national accounts. While overall income inequality rose over the past five decades, the rise in overall consumption inequality was small. The declining quality of income data likely contributes to these differences for the bottom of the distribution. Asset price changes likely account for some of the differences in recent years for the top of the distribution.

Previous version in 2017 (with a much longer abstract): Consumption and Income Inequality in the U.S. Since the 1960s. Bruce D. Meyer & James X. Sullivan. NBER Working Paper 23655. Aug 2017. https://www.bipartisanalliance.com/2017/08/consumption-and-income-inequality-in-us.html

People relied too much on their self-perceptions, which were more negative than the impressions they made; & understood that others saw them more positively than how they saw themselves, but they did not understand the extent of this positivity

Elsaadawy, N., & Carlson, E. N. (2022). Do you make a better or worse impression than you think? Journal of Personality and Social Psychology, Aug 2022. https://doi.org/10.1037/pspp0000434

Abstract: Are people’s metaperceptions, or their beliefs about how others perceive them, too positive, too negative, or spot on? Across six samples of new acquaintances (total N = 1,113) and/or well-known acquaintances (total N = 1,336), we indexed metabias (i.e., the mean-level difference between metaperceptions and impressions) on a broad range of attributes to test: (a) how biased people are on average, (b) whether bias is pervasive or limited to particular contexts (level of acquaintanceship) or attributes (e.g., liking judgments or traits), (c) whether bias is consistent across attributes, and (d) what explains bias. On average, participants demonstrated a negative metabias on most attributes for both new and well-known acquaintances, suggesting that people generally fail to appreciate how positively they are seen by others. However, there was variability around this average such that, whereas most participants were negatively biased (48%), many were accurate (34%), and some were positively biased (18%). Bias was also consistent across traits, suggesting that knowing people’s metabias for one attribute offers some insight into their relative bias for other attributes. What explained metabias? Generally, people relied too much on their self-perceptions, which were more negative than the impressions they made, although bias for new acquaintances involved additional factors. That said, people understood that others saw them more positively than how they saw themselves, but they did not understand the extent of this positivity. These results offer a general framework for understanding metabias and add to the growing literature, demonstrating that people are not positively biased. 

Rolf Degen summarizing... Sociologists conduct comparatively very few replications, but it looks like it would turn out badly if they did

Reproducibility in the Social Sciences. James W. Moody et al. Annual Review of Sociology, Vol. 48:65-85 (July 2022). https://doi.org/10.1146/annurev-soc-090221-035954

Abstract: Concern over social scientists’ inability to reproduce empirical research has spawned a vast and rapidly growing literature. The size and growth of this literature make it difficult for newly interested academics to come up to speed. Here, we provide a formal text modeling approach to characterize the entirety of the field, which allows us to summarize the breadth of this literature and identify core themes. We construct and analyze text networks built from 1,947 articles to reveal differences across social science disciplines within the body of reproducibility publications and to discuss the diversity of subtopics addressed in the literature. This field-wide view suggests that reproducibility is a heterogeneous problem with multiple sources for errors and strategies for solutions, a finding that is somewhat at odds with calls for largely passive remedies reliant on open science. We propose an alternative rigor and reproducibility model that takes an active approach to rigor prior to publication, which may overcome some of the shortfalls of the postpublication model.

Keywords: data replication, reproducibility

Deadly fungus can multiply by having sex, which could produce more drug-resistant, virulent strains

Yue Wang, Jianping Xu. Population genomic analyses reveal evidence for limited recombination in the superbug Candida auris in nature. Computational and Structural Biotechnology Journal, 2022; 20: 3030 DOI: 10.1016/j.csbj.2022.06.030

Abstract: Candida auris is a recently emerged, multidrug-resistant pathogenic yeast capable of causing a diversity of human infections worldwide. Genetic analyses based on whole-genome sequences have clustered strains in this species into five divergent clades, with each clade containing limited genetic variation and one of two mating types, MTLa or MTLα. The patterns of genetic variations suggest simultaneous emergence and clonal expansion of multiple clades of this pathogen across the world. At present, it is unclear whether recombination has played any role during the evolution of C. auris. In this study, we analyzed patterns of associations among single nucleotide polymorphisms in both the nuclear and the mitochondrial genomes of 1,285 strains to investigate potential signatures of recombination in natural C. auris populations. Overall, we found that polymorphisms in the nuclear and mitochondrial genomes clustered the strains similarly into the five clades, consistent with a lack of evidence for recombination among the clades after their divergence. However, variable percentages of SNP pairs showed evidence of phylogenetic incompatibility and linkage equilibrium among samples in both the nuclear and the mitochondrial genomes, with the percentages higher in the total population than those within individual clades. Our results are consistent with limited but greater frequency of recombination before the divergence of the clades than afterwards. SNPs at loci related to antifungal resistance showed frequencies of recombination similar to or lower than those observed for SNPs in other parts of the genome. Together, though very limited, evidence for the observed recombination for both before and after the divergence of the clades suggests the possibility for continuous genetic exchange in natural populations of this important yeast pathogen.

4. Discussions

In this study, we analyzed the whole genome SNPs of 1,286 C. auris strains collected from across the world over the past 20+ years to investigate the potential signatures of recombination in this species. SNPs in both the nuclear and mitochondrial genomes were analyzed, both in the total sample as well as for each of the four clades where multiple strains have been sequenced. Our analyses revealed signatures of infrequent recombination in both the total sample as well as within each of the four individual clades. In addition, specific groups of SNPs, including those in genes involved in antifungal drug resistance as well as those that are shared among all four clades, were separately analyzed to help identify the potential contributors to the observed signatures of recombination. Different patterns of allelic associations were found among the sample types and between the nuclear and mitochondrial genomes. Below we discuss the main findings of our analyses and the major implications of our results.

4.1. Comparison between nuclear and mitochondrial genomes

The 1,285 genomes analyzed here represented all the strains of C. auris that have been sequenced and deposited in GenBank by researchers, up to May 2022. Multiple studies have analyzed variable numbers of strains, with the largest number of strains analyzed by Muñoz et al. [20] where 304 strains from many geographic regions were included. Most studies have focused on nuclear genomes. Analyses of nuclear genomes in those studies revealed that the global population of C. auris could be grouped into five distinct clades, with Clades I to IV represented by multiple strains in each while Clade V was represented by only one whole-genome sequenced strain (so far). However, one previous study analyzed mitogenome variations. Based on mitogenome SNPs of 130 C. auris strains, Misas et al. [69] showed that the mitogenome and nuclear genome SNPs clustered the strains into four similar clades. However, their analyses included only one Clade II strain and their results based on 10 Clade III strains from South Africa revealed no mitogenome sequence variation within Clade III. Our analyses here significantly expanded the sample sizes of all four clades with a total of 1,285 strains. While a similar pattern of sequence divergence within C. auris into five clades for both the nuclear genome and the mitochondrial genome was observed as previously reported (20,70), our analyses also revealed several notable features. Specifically, first, despite having more than twice as many strains as the earlier study (210 vs 86), we found no unambiguous SNP within the mitogenome of Clade IV, similar to that found by Misas et al. [69]. Second, the inclusion of 23 additional Clade II strains (versis one strain in the Misas et al. study) revealed no mitogenome SNP within Clade II. Third, the inclusion of 504 additional strains from more diverse geographic sources in Clade III (i.e., 514 in this study vs 10 in the Misas et al study) revealed abundant mitogenome SNPs within Clade III. Together, these analyses revealed that the amounts of sequence variations between the nuclear and mitochondrial genomes differed at both the whole species as well as within individual clades. At the whole species level, the SNP frequency in the nuclear genome was 1.876% (232,179/12.37×106), about six times of that of the mitochondrial genome (0.315%; 89/28212).

The lower observed genetic variation in the mitochondrial genome than in the nuclear genome has been reported in several other fungal species, including the human pathogen Cryptococcus gattii species complex and the ectomycorrhizal mushroom Tricholoma matsutake species complex [71], [72], [73]. However within individual clades, while two clades (Clades II and IV) showed limited to no mitochondrial SNPs (consistent with the overall pattern within the species), the remaining two clades (Clades I and III) showed greater mitochondrial SNP frequencies than their respective nuclear genomes. At present, the mechanisms for the different amounts of sequence diversity between the two genomes among the clades are unknown. The small sample size and limited ecological niches (mostly from ear discharges) might have contributed to no mitochondrial sequence variation in Clade II. However, this explanation cannot hold for Clade IV where 210 strains from four continents and a variety of human body sites were examined, similar to those of Clades I and III strains in this study (Table S1). Geographically, strains of Clades II and IV are predominantly found in East Asia and the Americas respectively while Clades I and III are predominantly from South Asia and Africa respectively. It is possible that the higher temperature and other potential environmental factors in South Asia and Africa may have contributed to the higher mutation rates in mitochondrial genomes than in nuclear genomes in Clades I and III. The mechanisms for the observed divergent mitochondrial vs nuclear genetic variations among the four clades within C. auris remain to be elucidated.

4.2. Evidence of recombination

At both the species and individual clade levels, though the frequencies were generally low, evidence for PI was observed in both the nuclear and the mitochondrial genomes, with a significant proportion of those PI SNP pairs also in linkage equilibrium. However, the frequencies of PI SNP pairs differed among the samples. Overall, the frequency of nuclear PI SNP pairs at the species level was from twice to over 30 times of those within individual clades (Table 3, Table 4). A similar pattern was also observed for the mitochondrial genome SNPs. Together, these results suggested that there was more frequent recombination before the divergence of the clades than after individual clades were established. Specifically, though signatures of recombination were also detected within each of the four clades after their respective divergence, clonal reproduction and expansion seemed more dominant in natural populations of C. auris after the divergence of clades than before their divergence. Our observed pattern is largely consistent with the expectations of each clade having only one mating type and therefore less likely to mate and recombine among strains of the same clade.

Relative to the frequent reports of recombination in the nuclear genomes of fungal populations, reports of mitochondrial genome recombination are still rare. However, the list of fungal species and populations showing evidence of mitogenome recombination is growing. For example, since 1998, mitochondrial DNA recombination has been reported for the honey mushroom Armillaria gallica [74], the commercial button mushroom Agaricus bisporus [75], the wild ectomycorrhizal mushroom Russula virescens species complex [76], and the opportunistic human fungal pathogen Cryptococcus gattii species complex [71]. In the commercial mushroom A. bisporus, the observed frequency of mitochondrial loci with PI was correlated with the life cycles of two varieties within the species, with the outcrossing heterothallic population showing more evidence of mitochondrial genome recombination than the secondarily homothallic populations [75].

Because the ancestral population of C. auris contained strains of both mating types, evidence for recombination in the total sample was expected. The higher rate of SNP pairs that showed evidence for PI than those within individual clades is consistent with sexual recombination in the ancient population of this species. The absence of incongruent relationships among clades between nuclear and mitochondrial genome phylogenies is consistent with the absence of mating and recombination among the four clades after their divergence from each other. However, the observed PIs among SNP pairs within individual clades after their divergence are puzzling. Specifically, each clade is known to contain strains of only one mating type, MTLa for Clades I and IV, and MTLα for Clades II and III. In addition, we found limited evidence of parallel mutations in the genes that are most likely under parallel selective pressure, the antifungal drug resistance-related genes. While we cannot completely exclude the possibility that convergent mutations might have contributed to some of the observed PIs, our analyses revealed that even if they existed, such an effect would likely be minimal. However, evidence for recombination have been found in natural fungal populations known to contain only a single mating type. For example, same-sex mating has been reported in the human fungal pathogen Cryptococcus neoformans species complex and such mating can generate genetic recombinants, similar to what have been reported for opposite-sex mating and to natural populations containing strains of both mating types [77]. It is possible that low-frequency same-sex mating could have similarly happened to the individual C. auris clades to generate the observed PIs and linkage equilibrium. Alternatively, low frequency strains of the alternative mating type may exist within each of the four clades in nature and mating between strains of opposite mating types could have generated the observed signatures of recombination. Indeed, these two possibilities are not mutually exclusive, and both could have contributed to the observed signatures of recombination. Broader and more intensive sampling as well as experimental investigations of genetic crosses are needed in order to test these two possibilities.

4.3. Genes adjacent to clade-shared SNPs

Our analyses revealed three clade-shared SNP regions, with SNPs in two of these regions showing high frequency of PI with other SNPs in the genome. Interestingly, all three clade-shared SNP regions are in intergenic regions between genes coding for hydrolases, oxidoreductases, and transcription factors with potential impacts on cell growth and lifespan (Table 7). For example, the ortholog of B9J08_000508, the downstream gene of clade-shared SNP region 1, is known to regulate the target of rapamycin complex 1 (TORC1) signaling. TORC1 is a multiprotein signaling complex functions as the organizer that incorporate internal and external cues to regulate cell growth and cell cycle progression [78]. A recent study demonstrated that TORC1 signaling plays an important role in controlling NaCl resistance through Sir2 in Saccharomyces cerevisiae [79]. The clade-shared SNPs within the upstream region of TORC1 gene may be involved in regulating the expression levels of TORC1.

Interestingly, the downstream gene of clade-shared SNP region 2, B9J08_002254, codes for a protein containing a putative FMN-binding domain which is known to be most frequently found in bacteria. It has been hypothesized that proteins containing such a domain in fungi may have been horizontally transferred from bacterial to fungal genomes [80]. Indeed, multiple independent transfers of such genes and the associated upstream sequences from bacteria to strains of C. auris in different clades could have contributed to the observed distributions of clade-shared polymorphisms and PIs. Our BLAST searches revealed that based on the amino acid sequence, the closest match to B9J08_002254 was in the bacterial genus Achromobacter, with a 99% query coverage and an E value of 1e-54.

The two genes located upstream and downstream of the clade-shared SNP region #3 were B9J08_003771 and B9J08_003772. Gene B9J08_003771 has a predicted unfolded protein-binding activity, while B9J08_003772 has a predicted DNA-binding transcription factor activity, zinc ion binding activity, and transcriptional regulation activity. The unfolded protein response is known to help human fungal pathogens survive in the host through balancing the load of proteins entering the endoplasmic reticulum and the protein-folding capacity of the organelle [81]. For example, in C. albicans, the zinc finger protein CZF1 is one of the DNA-binding proteins of the Cys6Zn2 class of transcriptional regulators with a multitude of functions such as biofilm induction, hyphal growth regulation, white-opaque switch, and yeast cell adherence [82], [83], [84], [85], [86]. While functionally likely important, how the polymorphisms in the intergenic regions of these two genes contribute to strain and population fitness remains to be investigated.

4.4. Conclusions and perspectives

This study identified limited but unambiguous evidence of recombination in both the total sample and within individual clades. In addition, evidence of recombination was found in both the nuclear and mitochondrial genomes, as well as between the nuclear and mitochondrial genomes. Overall, signatures of recombination were more prominent in the total sample than within individual clades, consistent with greater frequencies of recombination before the divergence of the four clades than after their divergence. At present, while several possibilities were suggested, the mechanism(s) for the observed recombination is not known. Nevertheless, the signatures of recombination identified here suggested a number of avenues from which further investigations could be conducted, including more extensive sampling for alternative mating types within each clade, laboratory attempts of both same-sex and opposite-sex mating, and identifying the adaptive significance of clade-shared SNPs. Such investigations should allow us to better understand the genetic architecture of virulence and drug resistance evolution within and among the divergent clades of this pathogen in natural and clinical environments.