High histone variant H3.3 content in mouse prospermatogonia suggests a role in epigenetic reformatting |
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Authors: | Michelle C. W. Tang Steve Binos Eng K. Ong Lee H. Wong Jeffrey R. Mann |
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Affiliation: | 1. Department of Zoology, The University of Melbourne, Gate 12 Royal Parade, Parkville, VIC, 3010, Australia 2. Genetics Theme, Murdoch Childrens Research Institute, Royal Children’s Hospital, Flemington Road, Parkville, VIC, 3052, Australia 3. Department of Primary Industries, Biosciences Research Division, 1 Park Drive, Bundoora, VIC, 3083, Australia 4. Scientific Services, Murdoch Childrens Research Institute, Royal Children’s Hospital, Flemington Road, Parkville, VIC, 3052, Australia 5. Department of Biochemistry and Molecular Biology, Monash University, Melbourne, VIC, 3800, Australia
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Abstract: | Histone variants can incorporate into the nucleosome outside of S-phase. Some are known to play important roles in mammalian germ cell development, this cell lineage being characterized by long phases of quiescence, a protracted meiotic phase, and genome-wide epigenetic reformatting events. The best known example of such an event is the global-scale erasure of DNA methylation in sexually indifferent primordial germ cells, then its re-establishment in fetal prospermatogonia and growing oocytes. Histone H3 and its post-translationally modified forms provide important waypoints in the establishment of epigenetic states. Using mass spectrometry and immunoblotting, we show that the H3.3 replacement variant is present at an unusually high amount in mouse prospermatogonia at the peak stage of global DNA methylation re-establishment. We speculate that H3.3 facilitates this process through achieving a greater level of accessibility of chromatin modifiers to DNA. |
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