Journal
CELL REPORTS
Volume 1, Issue 6, Pages 730-740Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2012.05.006
Keywords
-
Categories
Funding
- la Ligue Nationale contre le Cancer
- European Commission Network of Excellence EpiGeneSys [HEALTH-F4-2010-257082]
- ERC [2009-AdG_20090506]
- Canceropole INCa
- Ministere de l'Enseignement Superieur et de la Recherche/University Pierre et Marie Curie (UPMC), Paris, France
Ask authors/readers for more resources
Discovering how histone variants that mark distinct chromatin regions affect a developmental program is a major challenge in the epigenetics field. To assess the importance of the H3.3 histone variant and its dedicated histone chaperone HIRA, we used an established developmental model, Xenopus laevis. After the early rapid divisions exploiting a large maternal pool of both replicative H3.2 and replacement H3.3, H3.3 transcripts show a distinct peak of expression at gastrulation. Depletion of both H3.2 and H3.3 leads to an early gastrulation arrest. However, with only H3.3 depletion, defects occur at late gastrulation, impairing further development. Providing exogenous H3.3 mRNAs, but not replicative H3.2 mRNAs, rescues these defects. Notably, downregulation of the H3.3 histone chaperone HIRA similarly impairs late gastrulation, and we find a global defect in H3.3 incorporation into chromatin comparable to H3.3 depletion. We discuss how specific HIRA-dependent H3.3 deposition is required for chromatin dynamics during gastrulation.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available