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Originally published In Press as doi:10.1074/jbc.M603822200 on January 5, 2007
J. Biol. Chem., Vol. 282, Issue 10, 6936-6945, March 9, 2007
Human SSRP1 Has Spt16-dependent and -independent Roles in Gene Transcription*
Yanping Li,
Shelya X. Zeng,
Igor Landais, and
Hua Lu1
From the
Department of Biochemistry and Molecular Biology, Oregon Health & Science University, Portland, Oregon 97239
The facilitating chromatin transcription (FACT) complex, a heterodimer of SSRP1 and Spt16, has been shown to regulate transcription elongation through a chromatin template in vitro and on specific genes in cells. However, its global role in transcription regulation in human cells remains largely elusive. We conducted spotted microarray analyses using arrays harboring 8308 human genes to assess the gene expression profile after knocking down SSRP1 or Spt16 levels in human non-small cell lung carcinoma (H1299) cells. Although the changes of these transcripts were surprisingly subtle, there were 170 genes whose transcript levels were either reduced or induced >1.5-fold. Approximately 106 genes with >1.2-fold change at the level of transcripts were the common targets of both SSRP1 and Spt16 ( 1.3%). A subset of genes was regulated by SSRP1 independent of Spt16. Further analyses of some of these genes not only verified this observation but also identified the serum-responsive gene, egr1, as a novel target for both SSRP1 and Spt16. We further showed that SSRP1 and Spt16 are important for the progression of elongation RNA pol II on the egr1 gene. These results suggest that SSRP1 has Spt16-dependent and -independent roles in regulating gene transcription in human cells.
Received for publication, April 20, 2006
, and in revised form, January 5, 2007.
* This work was supported by NCI Grants CA93614, CA095441, and CA079721 from the National Institutes of Health (to H. L.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
The on-line version of this article (available at http://www.jbc.org) contains supplemental Figs. S1 and S2.
1 To whom correspondence should be addressed: Dept. of Biochemistry and Molecular Biology/L224, Oregon Health & Science University, 3181 SW Sam Jackson Park Rd., Portland, OR 97239. Tel.: 503-494-7414; E-mail: luh{at}ohsu.edu.

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Copyright © 2007 by the American Society for Biochemistry and Molecular Biology.
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