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We review the phenomenon of condition-dependent sex—where individuals' condition affects the likelihood that they will reproduce sexually rather than asexually. In recent years, condition-dependent sex has been studied both theoretically and empirically. Empirical results in microbes, fungi and plants support the theoretical prediction that negative condition-dependent sex, in which individuals in poor condition are more likely to reproduce sexually, can be evolutionarily advantageous under a wide range of settings. Here, we review the evidence for condition-dependent sex and its potential implications for the long-term survival and adaptability of populations. We conclude by asking why condition-dependent sex is not more commonly observed, and by considering generalizations of condition-dependent sex that might apply even for obligate sexuals. This article is part of the themed issue ‘Weird sex: the underappreciated diversity of sexual reproduction’.

Because mutations are mostly deleterious, mutation rates should be reduced by natural selection. However, mutations also provide the raw material for adaptation. Therefore, evolutionary theory suggests that the mutation rate must balance between adaptability—the ability to adapt—and adaptedness—the ability to remain adapted. We model an asexual population crossing a fitness valley and analyse the rate of complex adaptation with and without stress-induced mutagenesis (SIM)—the increase of mutation rates in response to stress or maladaptation. We show that SIM increases the rate of complex adaptation without reducing the population mean fitness, thus breaking the evolutionary trade-off between adaptability and adaptedness. Our theoretical results support the hypothesis that SIM promotes adaptation and provide quantitative predictions of the rate of complex adaptation with different mutational strategies.

Stress-induced mutagenesis has been observed in multiple species of bacteria and yeast. It has been suggested that in asexual populations, a mutator allele that increases the mutation rate during stress can sweep to fixation with the beneficial mutations it generates. However, even asexual microbes can undergo horizontal gene transfer and rare recombination, which typically interfere with the spread of mutator alleles. Here we examine the effect of horizontal gene transfer on the evolutionary advantage of stress-induced mutator alleles. Our results demonstrate that stress-induced mutator alleles are favored by selection even in the presence of horizontal gene transfer and more so when the mutator alleles also increase the rate of horizontal gene transfer. We suggest that when regulated by stress, mutation and horizontal gene transfer can be complementary rather than competing adaptive strategies and that stress-induced mutagenesis has important implications for evolutionary biology, ecology, and epidemiology, even in the presence of horizontal gene transfer and rare recombination.

Background Dispersal is a major factor in ecological and evolutionary dynamics. Although empirical evidence shows that the tendency to disperse varies among individuals in many organisms, the evolution of dispersal patterns is not fully understood. Previous theoretical studies have shown that condition-dependent dispersal may evolve as a means to move to a different environment when environments are heterogeneous in space or in time. However, dispersal is also a means to genetically diversify offspring, a genetic advantage that might be particularly important when the individual fitness is low. We suggest that plasticity in dispersal, in which fit individuals are less likely to disperse (Fitness-Associated Dispersal, or FAD), can evolve due to its evolutionary advantages even when the environment is homogeneous and stable, kin competition is weak, and the cost of dispersal is high. Results Using stochastic simulations we show that throughout the parameter range, selection favors FAD over uniform dispersal (in which all individuals disperse with equal probability). FAD also has significant long-term effects on the mean fitness and genotypic variance of the population. Conclusions We show that FAD evolves under a very wide parameter range, regardless of its effects on the population mean fitness. We predict that individuals of low quality will have an increased tendency for dispersal, even when the environment is homogeneous, there is no direct competition with neighbors, and dispersal carries significant costs.

Mobility coupling effects due to remote Coulomb scattering (RCS) are demonstrated for the first time in FD-SOI CMOS devices subjected to front and back interface electrical degradation. The evolution with stress time of the front and back threshold voltages as well as of the low field mobility values has been obtained. The front and back interface mobility degradations were then correlated to the stress induced interfacial charge variations for each stressed interface. This enabled the clear demonstration of the existence of mobility coupling effects between the front and back interface by RCS through the silicon film.

Individuals often vary markedly in their ability to cope with stressors, but the drivers of this variation remain poorly understood. Many studies have tested relationships among individual variation in glucocorticoid levels and the response to challenges—often finding inconsistent patterns; however, few have addressed whether variation in the capacity to terminate the stress response through negative feedback is associated with stress resilience. While conceptual models predict that interactions among different components of hypothalamic–pituitary–adrenal (HPA) axis regulation may be important predictors of the phenotypic and fitness effects of stress, we are aware of no previous experimental tests of this hypothesis. We investigate whether individual variation in HPA axis regulation is related to resilience to experimental challenges in free‐living tree swallows (Tachycineta bicolor). We mimicked salient natural challenges by temporarily reducing flight efficiency or increasing perceived predation risk during incubation, and determined whether HPA axis responsiveness prior to treatments predicted resilience. Females that exhibited both a robust HPA axis activation and strong negative feedback were less likely to abandon nests during incubation. Our results suggest that exhibiting a strong HPA axis activation coupled with effective negative feedback may predict stress resilience. Therefore, the ability to turn on and then off the HPA axis efficiently may be important for fitness. Our results also suggest that the interactions between different components of the HPA axis may provide greater insight into differences in stress coping capacity. A plain language summary is available for this article. Plain Language Summary

Aims Takotsubo cardiomyopathy (TC) is characterized by transient ventricular impairment, often preceded by emotional or physical stress. Racial differences affect the outcomes of several cardiovascular conditions; however, the effect of race on TC remains unknown. This investigation aims to assess the effect of race on in‐hospital outcomes of TC in a large national sample. Methods and results We conducted a US‐wide analysis of TC hospitalizations from 2006 to 2014 by querying the National Inpatient Sample database for the International Classification of Diseases‐ninth Revision TC code, characteristics, and inpatient outcomes. Patients with a primary diagnosis of acute coronary syndrome were excluded to reduce selection bias. Caucasians were compared with African Americans (AA) for differences in baseline characteristics and in‐hospital outcomes. Multivariate regression models were created to adjust for potential confounders. Of 97 650 TC patients, 83 807 (86.9%) were women, 89 624 (91.8%) identified as Caucasians, and 8026 (8.2%) as AA. The annual number of TC hospitalizations increased significantly from 2006 to 2014 in both races (from 335 to 21 265 annual cases, P < 0.001). In‐hospital mortality initially increased (1–2% in 2006 to 5–6% in 2009, P < 0.001) and subsequently remained relatively stable around 5–7% with no significant difference between races. In unadjusted analysis, AA had more cardiac arrests [304 (3.8%) vs. 2569 (2.9%), P = 0.04], invasive mechanical ventilation [1671 (20.8%) vs. 15 897 (17.7%), P = 0.002], tracheostomies [242 (3%) vs. 1600 (1.8%), P = 0.001], acute kidney injuries [1765 (22%) vs. 14 608 (16.3%), P < 0.0001], and longer hospital stays [4.5 (3.2–4.8) vs. 3.8 (3.7–3.9) days, P < 0.0001] compared with Caucasians. After the adjustment for differences in age, gender, comorbidities (using the enhanced Charlson comorbidity index), hospital location/teaching status, and socio‐economic factors, all differences were significantly attenuated or eliminated. Additionally, the adjusted risk was lower in AA compared with Caucasians, for cardiogenic shock [odds ratio (OR) 0.61 (0.47–0.78), P < 0.0001], mechanical ventilation [OR 0.8 (0.70–0.92), P = 0.002] and intraaortic balloon pump insertion [OR 0.63 (0.41–0.99), P = 0.04]. Conclusions Our investigation is the first large US‐wide analysis studying racial variations in TC outcomes. AA overall have more in‐hospital complications; however, the differences are driven by racial disparities in demographics, comorbidities, and socio‐economic factors.

The controversial theory of adaptive amplification states gene amplification mutations are induced by selective environments where they are enriched due to the stress caused by growth restriction on unadapted cells. We tested this theory with three independent assays using an Acinetobacter baylyi model system that exclusively selects for cat gene amplification mutants. Our results demonstrate all cat gene amplification mutant colonies arise through a multistep process. While the late steps occur during selection exposure, these mutants derive from low-level amplification mutant cells that form before growth-inhibiting selection is imposed. During selection, these partial mutants undergo multiple secondary steps generating higher amplification over several days to multiple weeks to eventually form visible high-copy amplification colonies. Based on these findings, amplification in this Acinetobacter system can be explained by a natural selection process that does not require a stress response. These findings have fundamental implications to understanding the role of growth-limiting selective environments on cancer development. We suggest duplication mutations encompassing growth factor genes may serve as new genomic biomarkers to facilitate early cancer detection and treatment, before high-copy amplification is attained.

Takotsubo syndrome (TS), also known as stress-induced cardiomyopathy, is classically characterized by an acute onset mimicking myocardial infarction and by distinctive transient wall motion abnormalities detectable via echocardiography, often resembling a Japanese octopus trap (the so-called “takotsubo”). The possibility that a genetic background may contribute to TS susceptibility emerged early, supported by several familial case reports. Despite a large number of investigations, no definitive genetic markers associated with TS risk have been conclusively identified. The lack of a clear Mendelian inheritance pattern suggests a multifactorial etiology and pathogenesis, likely involving complex gene–environment interactions and a polygenic background. This review analyzes the genetic variants implicated in the different functional pathways contributing to TS pathogenesis and discusses the current state of knowledge regarding its genetic underpinnings. Finally, we propose future directions for research aimed at identifying a multigene susceptibility panel that could be useful in diagnosis, prevention strategies, and the identification of novel therapeutic targets for individuals at high risk. We conclude that innovative approaches based on data-mining algorithms and nonlinear analytic methods applied to large patient datasets may be instrumental in resolving the genetic complexity of TS.

Abstract BACKGROUND: Stress-induced cardiomyopathy (SIC) is a poorly understood condition associated with periods of emotional and physical stress. The clinical approaches for management of SIC are supportive and reactive to patient symptoms. OBJECTIVE: To utilize next-generation exome sequencing to define genetic variation associated with, and potentially responsible for, this disease. METHODS: We performed exome sequencing of 7 white female patients with SIC. Filtering of the identified variants was performed to limit our investigation to those sequences that passed quality control criteria, were rare or novel, were determined algorithmically to have high impact on the associated protein, and were within regions of high species conservation. All variants were verified by using Sanger sequencing. RESULTS: Exome-sequencing analysis revealed that each patient carried predicted deleterious variants affecting known cardiomyopathy genes. In each case, the identified variant was either not previously found in public human genome data or was previously annotated in a database of clinical variants associated with cardiac dysfunction. CONCLUSION: Patients with SIC harbor deleterious mutations in established cardiomyopathy genes at a level higher than healthy controls. We hypothesize that patients at highest risk for SIC likely live in a compensated state of cardiac dysfunction that manifests clinically only after the myocardium is stressed. In short, we propose that SIC is another example of an occult cardiomyopathy with a distinct physiological trigger and suggest that alternative clinical approaches to these patients may be warranted.