Genome-wide Analysis of YY2 Versus YY1 Target Genes

DSpace/Manakin Repository

Genome-wide Analysis of YY2 Versus YY1 Target Genes

Citable link to this page

. . . . . .

Title: Genome-wide Analysis of YY2 Versus YY1 Target Genes
Author: Coser, Kathryn R.; Chen, Li; Shioda, Toshihiro; Lynch, Mary C.; Yang, Chuanwei; Schmidt, Emmett Vance

Note: Order does not necessarily reflect citation order of authors.

Citation: Chen, Li, Toshi Shioda, Kathryn R. Coser, Mary C. Lynch, Chuanwei Yang, and Emmett V. Schmidt. 2010. Genome-wide analysis of YY2 versus YY1 target genes. Nucleic Acids Research 38(12): 4011-4026.
Full Text & Related Files:
Abstract: Yin Yang 1 (YY1) is a critical transcription factor controlling cell proliferation, development and DNA damage responses. Retrotranspositions have independently generated additional YY family members in multiple species. Although Drosophila YY1 [pleiohomeotic (Pho)] and its homolog [pleiohomeotic-like (Phol)] redundantly control homeotic gene expression, the regulatory contributions of YY1-homologs have not yet been examined in other species. Indeed, targets for the mammalian YY1 homolog YY2 are completely unknown. Using gene set enrichment analysis, we found that lentiviral constructs containing short hairpin loop inhibitory RNAs for human YY1 (shYY1) and its homolog YY2 (shYY2) caused significant changes in both shared and distinguishable gene sets in human cells. Ribosomal protein genes were the most significant gene set upregulated by both shYY1 and shYY2, although combined shYY1/2 knock downs were not additive. In contrast, shYY2 reversed the anti-proliferative effects of shYY1, and shYY2 particularly altered UV damage response, platelet-specific and mitochondrial function genes. We found that decreases in YY1 or YY2 caused inverse changes in UV sensitivity, and that their combined loss reversed their respective individual effects. Our studies show that human YY2 is not redundant to YY1, and YY2 is a significant regulator of genes previously identified as uniquely responding to YY1.
Published Version: doi://10.1093/nar/gkq112
Other Sources: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2896514/pdf/
Terms of Use: This article is made available under the terms and conditions applicable to Other Posted Material, as set forth at http://nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of-use#LAA
Citable link to this page: http://nrs.harvard.edu/urn-3:HUL.InstRepos:4737686

Show full Dublin Core record

This item appears in the following Collection(s)

 
 

Search DASH


Advanced Search
 
 

Submitters