Defective germline reprogramming rewires the spermatogonial transcriptome.

ABSTRACT: Defective germline reprogramming in Piwil4 (Miwi2)- and Dnmt3l-deficient mice results in the failure to reestablish transposon silencing, meiotic arrest and progressive loss of spermatogonia. Here we sought to understand the molecular basis for this spermatogonial dysfunction. Through a combination of imaging, conditional genetics and transcriptome analysis, we demonstrate that germ cell elimination in the respective mutants arises as a result of defective de novo genome methylation during reprogramming rather than because of a function for the respective factors within spermatogonia. In both Miwi2^-/- and Dnmt3l^-/- spermatogonia, the intracisternal-A particle (IAP) family of endogenous retroviruses is derepressed, but, in contrast to meiotic cells, DNA damage is not o

SUBMITTER: Vasiliauskaite L 

PROVIDER: S-EPMC6086329 | biostudies-literature | 2018 May

REPOSITORIES: biostudies-literature