scholarly journals Cockayne syndrome group B protein enhances elongation by RNA polymerase II

1997 ◽  
Vol 94 (21) ◽  
pp. 11205-11209 ◽  
Author(s):  
C. P. Selby ◽  
A. Sancar
2003 ◽  
Vol 23 (1) ◽  
pp. 382-388 ◽  
Author(s):  
Sung-Lim Yu ◽  
Sung-Keun Lee ◽  
Robert E. Johnson ◽  
Louise Prakash ◽  
Satya Prakash

ABSTRACT Abasic (AP) sites represent one of the most frequently formed lesions in DNA. Here, we examine the consequences of the stalling of RNA polymerase II at AP sites in DNA in Saccharomyces cerevisiae. A severe inhibition of transcription occurs in strains that are defective in the removal of AP sites and that also lack the RAD26 gene, a homolog of the human Cockayne syndrome group B (CSB) gene, and, importantly, a dramatic rise in mutagenesis is incurred in such strains. From the various observations presented here, we infer that the stalling of transcription at AP sites is highly mutagenic.


1997 ◽  
Vol 94 (9) ◽  
pp. 4306-4311 ◽  
Author(s):  
A. S. Balajee ◽  
A. May ◽  
G. L. Dianov ◽  
E. C. Friedberg ◽  
V. A. Bohr

2006 ◽  
Vol 26 (24) ◽  
pp. 9430-9441 ◽  
Author(s):  
Shisheng Li ◽  
Baojin Ding ◽  
Runqiang Chen ◽  
Christine Ruggiero ◽  
Xuefeng Chen

ABSTRACT Rpb9, a small nonessential subunit of RNA polymerase II, has been shown to have multiple transcription-related functions in Saccharomyces cerevisiae. These functions include promoting transcription elongation and mediating a subpathway of transcription-coupled repair (TCR) that is independent of Rad26, the homologue of human Cockayne syndrome complementation group B protein. Rpb9 is composed of three distinct domains: the N-terminal Zn1, the C-terminal Zn2, and the central linker. Here we show that the Zn1 and linker domains are essential, whereas the Zn2 domain is almost dispensable, for both transcription elongation and TCR functions. Impairment of transcription elongation, which does not dramatically compromise Rad26-mediated TCR, completely abolishes Rpb9-mediated TCR. Furthermore, Rpb9 appears to be dispensable for TCR if its transcription elongation function is compensated for by removing a transcription repression/elongation factor. Our data suggest that the transcription elongation function of Rpb9 is involved in TCR.


2005 ◽  
Vol 20 (2) ◽  
pp. 187-198 ◽  
Author(s):  
Altaf H. Sarker ◽  
Susan E. Tsutakawa ◽  
Seth Kostek ◽  
Cliff Ng ◽  
David S. Shin ◽  
...  

Cell ◽  
1995 ◽  
Vol 82 (4) ◽  
pp. 555-564 ◽  
Author(s):  
Karla A. Henning ◽  
Lei Li ◽  
Narayan Iyer ◽  
Lisa D. McDaniel ◽  
Michael S. Reagan ◽  
...  

Oncotarget ◽  
2016 ◽  
Vol 8 (7) ◽  
pp. 11004-11019 ◽  
Author(s):  
Jinshan He ◽  
Qianzheng Zhu ◽  
Gulzar Wani ◽  
Altaf A. Wani

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