UNASSIGNED: @entity2008 are common in the @entity1 population, causing germ cell loss at meiotic prophase I and @entity249 . The mechanisms driving this loss are unknown, but persistent meiotic DNA damage and asynapsis may be triggers. Here we investigate the contribution of these lesions to oocyte elimination in @entity19 with @entity2008 , e.g. @entity2689 ( @entity2689 ) and translocations. We show that asynapsed chromosomes trigger oocyte elimination at diplonema, which is linked to the presence of phosphorylated @entity6714 (yH2AFX). We find that DNA double-strand break (DSB) foci disappear on asynapsed chromosomes during pachynema, excluding persistent DNA damage as a likely cause, and demonstrating the existence in @entity1 oocytes of a repair pathway for asynapsis-associated DNA DSBs. Importantly, deletion or point mutation of @entity6714 restores oocyte numbers in @entity2689 females to wild type (XX) levels. Unexpectedly, we find that asynapsed supernumerary chromosomes do not elicit prophase I loss, despite being enriched for yH2AFX and other checkpoint proteins. These results suggest that oocyte loss cannot be explained simply by asynapsis checkpoint models, but is related to the gene content of asynapsed chromosomes. A similar mechanistic basis for oocyte loss may operate in @entity1 with @entity2008 .

Histone XXXX Links Meiotic Chromosome Asynapsis to Prophase I Oocyte Loss in Mammals.

@entity1 :: ('9606', 'Species') :: ['mammalian', 'humans', 'human'] @entity249 :: ('MESH:D007246', 'Disease') :: ['infertility'] @entity19 :: ('10090', 'Species') :: ['mice'] @entity2689 :: ('MESH:D014424', 'Disease') :: ['XO', 'Turner syndrome'] @entity2008 :: ('MESH:D002869', 'Disease') :: ['chromosome abnormalities', 'Chromosome abnormalities'] @entity6714 :: ('3014', 'Gene') :: ['H2afx', 'H2AFX']
@entity6714 :: (3014,Gene) :: ['H2AFX']
