L3MBTL2 is required for normal spermatogenesis and the maintenance of male fertility
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AbstractL3MBTL2 is a member of the MBT-domain proteins, which are involved in transcriptional repression and implicated in chromatin compaction. L3MBTL2 is found to regulate cell proliferation and differentiation in mouse embryonic stem cells and early embryonic development. Our previous study has shown that L3mbtl2 is highly expressed in the testis, but its role in spermatogenesis remains unclear. In the present study, we show that L3MBTL2 is highly expressed in pachytene spermatocytes. Germ cell-specific knockout of L3mbtl2 in the testis led to mice with smaller testes, increased abnormal spermatozoa and reduced sperm counts, and the mice ceased to produce progeny at a much earlier age. Mechanistically, L3mbtl2 deficiency resulted in inappropriate retention of γH2AX on autosomes, and defective crossing-over and synapsis during the pachytene stage of meiosis I, and more germ cell apoptosis and degeneration. Acetylation of H4, H2B and H3 in germ cells, and the subsequent protamine 1 deposition and chromatin condensation in sperm were reduced in L3mbtl2 deficient mice as compared with wild type mice. These results suggest that L3mbtl2 plays important roles in meiosis and germ cell survival, and in chromatin remodeling during spermiogenesis.
All Author(s) ListMeng CL, Liao JY, Zhao DF, Huang HH, Qin JZ, Lee TL, Chen DG, Chan WY, Xia Y
Name of ConferenceASBMB 2017 Annual Meeting
Start Date of Conference22/04/2017
End Date of Conference26/04/2017
Place of ConferenceChicago
Country/Region of ConferenceUnited States of America
LanguagesEnglish-United States

Last updated on 2018-20-01 at 19:19