Journal
DEVELOPMENT GROWTH & DIFFERENTIATION
Volume 50, Issue 5, Pages 321-330Publisher
WILEY
DOI: 10.1111/j.1440-169x.2008.01041.x
Keywords
acetyltransferase; chromatin; histone; Hox gene
Categories
Funding
- NCI NIH HHS [P30 CA016672, CA16672] Funding Source: Medline
- NICHD NIH HHS [R01 HD030284] Funding Source: Medline
- NIGMS NIH HHS [GM067718, R01 GM067718] Funding Source: Medline
Ask authors/readers for more resources
Histone acetylation plays important roles in gene regulation. However, the functions of individual histone acetyltransferases (HATs) in specific developmental transcription programs are not well defined. To define the functions of Gcn5, a prototypical HAT, during mouse development, we have created a series of mutant Gcn5 alleles. Our previous work revealed that deletion of Gcn5 leads to embryonic death soon after gastrulation. Embryos homozygous for point mutations in the catalytic center of Gcn5 survive longer, but die soon after E16.0 and exhibit defects in cranial neural tube closure. Embryos bearing a hypomorphic Gcn5(flox(neo)) allele also exhibit neural closure defects and die at or soon after birth. We report here that Gcn5(flox(neo)/flox(neo)) and Gcn5(flox(neo)/Delta) embryos exhibit anterior homeotic transformations in lower thoracic and lumbar vertebrae. These defects are accompanied by a shift in the anterior expression boundary of Hoxc8 and Hoxc9. These data provide the first evidence that Gcn5 contributes to Hox gene regulation and is required for normal anteroposterior patterning of the mouse skeleton.
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