Journal
DEVELOPMENTAL CELL
Volume 14, Issue 4, Pages 481-493Publisher
CELL PRESS
DOI: 10.1016/j.devcel.2008.01.018
Keywords
-
Categories
Funding
- NCI NIH HHS [R01 CA095542-02, R01 CA095542-03, CA95542, R01 CA095542, R01 CA095542-04, R01 CA095542-05] Funding Source: Medline
Ask authors/readers for more resources
Drosophila embryos are highly sensitive to gamma-ray-induced apoptosis at early but not later, more differentiated stages during development. Two proapoptotic genes, reaper and hid, are upregulated rapidly following irradiation. However, in post-stage-1 2 embryos, in which most cells have begun differentiation, neither proapoptotic gene can be induced by high doses of irradiation. Our study indicates that the sensitive-to-resistant transition is due to epigenetic blocking of the irradiation-responsive enhancer region (IRER), which is located upstream of reaper but is also required for the induction of hid in response to irradiation. This IRER, but not the transcribed regions of reaper/hid, becomes enriched for trimethylated H3K27/H3K9 and forms a heterochromatinlike structure during the sensitive-to- resistant transition. The functions of histone-modifying enzymes Hdac1 (rpd3) and Su(var)3-9 and PcG proteins Su(z)12 and Polycomb are required for this process. Thus, direct epigenetic regulation of two proapoptotic genes controls cellular sensitivity to cytotoxic stimuli.
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