Journal
CELL REPORTS
Volume 7, Issue 1, Pages 113-126Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2014.02.044
Keywords
-
Categories
Funding
- NIH Office of Research Infrastructure Programs [P40 OD010440]
- National Bioresource Project for the Experimental Animal Nematode C. elegans
- Helen Hay Whitney postdoctoral fellowship [T32-CAA009361]
- National Institute on Aging of the National Institute of Health (NIH) [K99AG043550]
- NRSA from the NIH/NIGMS [F32GM100515]
- EMBO Fellowship
- UNC Lineberger Comprehensive Cancer Center Basic Sciences Training Program [T32CA09156]
- American Cancer Society [PF-13-085-01-DMC]
- NIH [GM096194, GM068088, GM072551, GM058012, CA118487, MH096066]
- John and Virginia Kaneb Fellowship
- Charles E. W. Grinnell Fund
- Ellison Foundation Senior Scholar Award
Ask authors/readers for more resources
How epigenetic information is transmitted from generation to generation remains largely unknown. Deletion of the C. elegans histone H3 lysine 4 dimethyl (H3K4me2) demethylase spr-5 leads to inherited accumulation of the euchromatic H3K4me2 mark and progressive decline in fertility. Here, we identified multiple chromatin-modifying factors, including H3K4me1/me2 and H3K9me3 methyltransferases, an H3K9me3 demethylase, and an H3K9me reader, which either suppress or accelerate the progressive transgenerational phenotypes of spr-5 mutant worms. Our findings uncover a network of chromatin regulators that control the transgenerational flow of epigenetic information and suggest that the balance between euchromatic H3K4 and heterochromatic H3K9 methylation regulates transgenerational effects on fertility.
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