Captive breeding programs often use a pedigree to identify breeding pairs that maintain genetic diversity and limit inbreeding. However, unintentional breeding of closely related individuals can occur when errors exist in the pedigree and may subsequently result in inbreeding depression. In this study, a DNA-based approach was used to identify parentage assignment errors in the captive pedigree of the critically endangered Attwater's prairie-chicken Tympanuchus cupido attwateri, and tested whether clutch survival increased using DNA-relatedness values for assigning breeding pairs instead of the pedigree and mean kinship. Parentage assignment error was observed in each year surveyed ranging from 2.4 to 7.3%. After correcting identified errors prior to the 2013 breeding season, 11 of 38 assigned pedigree-based breeding pairs still possessed DNA-based relatedness coefficients (r DNA ) ≥0.125 suggesting that additional errors remained in the pedigree. Two approaches were used to prevent breeding among close relatives in 2013 and 2014. Assigned pedigree-based breeding pairs in 2013 that possessed r DNA ≥0.125 were reassigned unrelated breeding partners, while all individuals in 2014 were used to identify the minimum overall r DNA for the breeding population without reference to the pedigree other than to verify founder representation. Both years resulted in a significant reduction in mean parental relatedness among chicks (P < 0.001) and a significant increase in the proportion of the clutch surviving to 5 weeks post-hatch (P ≤ 0.006) compared to 2012 when breeding pairs were assigned using only the pedigree. No significant difference in the proportion of the clutch surviving was observed between 2013 and 2014 (P > 0.300). These results have important implications for the captive management of endangered species, and highlight the importance of periodically evaluating for pedigree errors. To what degree pedigree errors limit fitness in other endangered species captive populations deserves further attention.

In eukaryotes, heterochromatin plays a critical role in organismal development and cell fate acquisition, through regulating gene expression. The evolutionarily conserved lysine-specific demethylases, Lsd1 and Lsd2, remove mono- and dimethylation on histone H3, serving complex roles in gene expression. In the fission yeast Schizosaccharomyces pombe, null mutations of Lsd1 and Lsd2 result in either severe growth defects or inviability, while catalytic inactivation causes minimal defects, indicating that Lsd1 and Lsd2 have essential functions beyond their known demethylase activity. Here, we show that catalytic mutants of Lsd1 or Lsd2 partially assemble functional heterochromatin at centromeres in RNAi-deficient cells, while the C-terminal truncated alleles of Lsd1 or Lsd2 exacerbate heterochromatin formation at all major heterochromatic regions, suggesting that Lsd1 and Lsd2 repress heterochromatic transcripts through mechanisms both dependent on and independent of their catalytic activities. Lsd1 and Lsd2 are also involved in the establishment and maintenance of heterochromatin. At constitutive heterochromatic regions, Lsd1 and Lsd2 regulate one another and cooperate with other histone modifiers, including the class II HDAC Clr3 and the Sirtuin family protein Sir2 for gene silencing, but not with the class I HDAC Clr6. Our findings explore the roles of lysine-specific demethylases in epigenetic gene silencing at heterochromatic regions.

Significance The process by which new complex traits evolve has been a persistent conundrum throughout the history of evolutionary inquiry. How multiple physiological changes at the organism level and genetic changes at the molecular level combine is still unclear for many traits. Here, we studied the displays of manakins, who beat their wings together at nearly twice the speed of other songbirds to produce a loud “snap” that attracts mates. We simultaneously analyzed evolution of gene expression levels and gene sequences to identify key genes related to muscle contractions and tissue regeneration after stress. Our results show how innovative behavioral traits evolve as a layered process where recent molecular shifts build on ancestral genetic evolutionary changes.

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