GSE126443
ANKRD31  regulates  spatiotemporal  patterning  of  meiotic  recombination  initiation  and    ensures recombination between heterologous sex chromosomes in mice
Orderly  segregation  of  chromosomes  during  meiosis  requires  that  crossovers  form  between  homologous  chromosomes  by  recombination.  Programmed  DNA  double-strand  breaks  (DSBs)  initiate  meiotic  recombination.  We  identify  ANKRD31  as  a  critical  component  of  complexes  of  DSB-promoting   proteins   which   assemble   on   meiotic   chromosome   axes.   Genome-wide,   ANKRD31  deficiency  causes  delayed  recombination  initiation.  In  addition,  loss  of  ANKRD31  alters  DSB  distribution  owing  to  reduced  selectivity  for  sites  that  normally  attract  DSBs.  Strikingly,  ANKRD31  deficiency  also  abolishes  uniquely  high  rates  of  recombination  that  normally   characterize   pseudoautosomal   regions   (PARs)   of   X   and   Y   chromosomes. Consequently,  sex  chromosomes  do  not  form  crossovers  leading  to  chromosome  segregation failure in ANKRD31-deficient spermatocytes. These defects are accompanied by a genome-wide delay  in  assembling  DSB-promoting  proteins  on  axes  and  a  loss  of  a  pecialized  PAR-axis  domain  that  is  highly  enriched  for  DSB-promoting  proteins.  Thus,  we  propose  a  model  for  spatiotemporal  patterning  of  recombination  by  ANKRD31-dependent  control  of  axis-associated  complexes of DSB-promoting proteins. Overall design: H3K4me3-ChIP-seq and DMC1-SSDS experiments were performed on testis from different mouse lines