The question of why females engage in extra-pair behaviors is long-standing in evolutionary biology. One suggestion is that these behaviors are maintained through pleiotropic effects on male extra-pair behaviors (genes controlling extra-pair reproduction are shared between sexes, but only beneficial to one sex, in this case, males). However, for this to evolve extra-pair reproduction must be both heritable and positively genetically correlated between sexes. Previous studies have suggested low heritability with no evidence for between-sex genetic correlations in extra-pair reproduction. However, these have not considered indirect genetic effects (derived from the behavior of others, IGEs) from the social partner, the influence of the social partner\'s genotype on the phenotype of an individual, despite the potential of IGEs to uncover hidden heritable variation. Using data from a closed-house sparrow population with a genetic pedigree spanning two decades, we tested the influence of social partner IGEs on heritable variation and genetic correlation estimates of extra-pair reproduction. We found that the inclusion of IGEs resulted in larger heritable genetic variance for both male and female extra-pair heritability. While IGEs did not change between-sex genetic correlations, we found they reduced uncertainty in those estimates. Future studies should consider the effect of IGEs on the mechanisms of sex-specific extra-pair reproduction.

Animal sociality, an individual\'s propensity to associate with others, has fitness consequences through mate choice, for example, directly, by increasing the pool of prospective partners, and indirectly through increased survival, and individuals benefit from both. Annually, fitness consequences are realized through increased mating success and subsequent fecundity. However, it remains unknown whether these consequences translate to lifetime fitness. Here, we quantified social associations and their link to fitness annually and over lifetime, using a multi-generational, genetic pedigree. We used social network analysis to calculate variables representing different aspects of an individual\'s sociality. Sociality showed high within-individual repeatability. We found that birds with more opposite-sex associates had higher annual fitness than those with fewer, but this did not translate to lifetime fitness. Instead, for lifetime fitness, we found evidence for stabilizing selection on opposite-sex sociality, and sociality in general, suggesting that reported benefits are only short-lived in a wild population, and that selection favors an average sociality.

Germline mutations in RUNX1 result in rare autosomal-dominant familial platelet disorder with predisposition to acute myeloid leukemia (FPD/AML). As genetic analysis is becoming increasingly prevalent, the diagnosis rate of FPD/AML is expected to increase. In this report, we present two pedigrees, one diagnosed molecularly and another highly suspected to be FPD/AML, whose members both received allogeneic hematopoietic stem cell transplantation (HSCT). Both pedigrees had a family history of thrombocytopenia, platelet dysfunction, and hematological malignancies. One family inherited a frameshift mutation (p.P240fs) of RUNX1, a known pathogenic variant. Another family inherited a point mutation (p.G168R) in the runt-homology domain, the clinical significance of which is uncertain at this point. As this mutation was completely absent from all population databases and had a relatively high REVEL score of 0.947, we thought that it would be dangerous to ignore its possible pathogenicity. Consequently, we avoided choosing HSCT donors from relatives of both families and performed HSCT from unrelated donors. In conclusion, our experience with two families of FPD/AML highlights the importance of searching for gene mutations associated with germline predisposition and indicates the necessity of developing a donor coordination system for FPD/AML patients, as well as a support system for families.

This report highlights case of two siblings who developed haemophagocytic lymphohystiocytosis due to distinct genetic abnormalities. Though their presentation was clinically similar, the cases demonstrate that a shared genetic diagnosis among siblings cannot be assumed.

Objective To explore the etiology of human oocyte maturation arrest in two infertile Chinese sisters. Methods Clinical examination and genetic testing of all available family members were conducted, and the findings were used to create a pedigree. Mutation screening using PCR amplification and DNA Sanger sequencing of the entire tubulin beta 8 class VIII gene ( TUBB8) including intron-exon boundaries was performed to identify mutations. Results A novel missense TUBB8 mutation (c.1054G > T, p.A352S) in the patient and her elder sister was detected and shown to be associated with oocyte maturation arrest. Conclusion Our findings expand the known mutation spectrum of TUBB8 and provide insights into the etiology of human oocyte maturation arrest.

A combination of mark-recapture and genetic sampling was used to extend the minimum longevity of an elasmobranch species and the life span estimate of the lemon shark Negaprion brevirostris was increased conservatively from 20·2 to 37 years. This increase in longevity means higher vulnerability and a longer recovery time from exploitation.