Journal
HUMAN MOLECULAR GENETICS
Volume 25, Issue 24, Pages 5300-5310Publisher
OXFORD UNIV PRESS
DOI: 10.1093/hmg/ddw344
Keywords
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Funding
- Medical Research Council UK [U117532009]
- EMBO
- BBSRC [BB/F007434/1, BB/J00877X/1, BB/N000463/1]
- University of Kent
- BBSRC [BB/N000463/1, BB/J00877X/1, BB/F007434/1] Funding Source: UKRI
- Biotechnology and Biological Sciences Research Council [BB/F007434/1, BB/N000463/1, BB/J00877X/1] Funding Source: researchfish
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During spermatogenesis, germ cells that fail to synapse their chromosomes or fail to undergo meiotic sex chromosome inactivation (MSCI) are eliminated via apoptosis during mid-pachytene. Previous work showed that Y-linked genes Zfy1 and Zfy2 act as 'executioners' for this checkpoint, and that wrongful expression of either gene during pachytene triggers germ cell death. Here, we show that in mice, Zfy genes are also necessary for efficient MSCI and the sex chromosomes are not correctly silenced in Zfy-deficient spermatocytes. This unexpectedly reveals a triple role for Zfy at the mid-pachytene checkpoint in which Zfy genes first promote MSCI, then monitor its progress (since if MSCI is achieved, Zfy genes will be silenced), and finally execute cells with MSCI failure. This potentially constitutes a negative feedback loop governing this critical checkpoint mechanism.
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