scholarly journals RNA Polymerase II Elongation Complexes Containing the Cockayne Syndrome Group B Protein Interact with a Molecular Complex Containing the Transcription Factor IIH Components Xeroderma Pigmentosum B and p62

1998 ◽  
Vol 273 (43) ◽  
pp. 27794-27799 ◽  
Author(s):  
Dean Tantin
Keyword(s):  
Transcription Factor ◽  
Rna Polymerase ◽  
Rna Polymerase Ii ◽  
Molecular Complex ◽  
Xeroderma Pigmentosum ◽  
Cockayne Syndrome ◽  
Group B

scholarly journals The Stalling of Transcription at Abasic Sites Is Highly Mutagenic

2003 ◽  
Vol 23 (1) ◽  
pp. 382-388 ◽  
Author(s):  
Sung-Lim Yu ◽  
Sung-Keun Lee ◽  
Robert E. Johnson ◽  
Louise Prakash ◽  
Satya Prakash
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Rna Polymerase ◽  
Rna Polymerase Ii ◽  
Cockayne Syndrome ◽  
Abasic Sites ◽  
Dramatic Rise ◽  
Ap Sites ◽  
Group B

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.

scholarly journals Reduced RNA polymerase II transcription in extracts of Cockayne syndrome and xeroderma pigmentosum/Cockayne syndrome cells

1997 ◽  
Vol 25 (18) ◽  
pp. 3636-3642 ◽  
Author(s):  
G. L. Dianov ◽  
J.-F. Houle ◽  
N. Iyer ◽  
V. A. Bohr ◽  
E. C. Friedberg
Keyword(s):  
Rna Polymerase ◽  
Rna Polymerase Ii ◽  
Xeroderma Pigmentosum ◽  
Cockayne Syndrome ◽  
Rna Polymerase Ii Transcription

scholarly journals Mechanism of Promoter Melting by the Xeroderma Pigmentosum Complementation Group B Helicase of Transcription Factor IIH Revealed by Protein-DNA Photo-Cross-Linking

2000 ◽  
Vol 20 (21) ◽  
pp. 8168-8177 ◽  
Author(s):  
Maxime Douziech ◽  
Frédéric Coin ◽  
Jean-Marc Chipoulet ◽  
Yoko Arai ◽  
Yoshiaki Ohkuma ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Rna Polymerase Ii ◽  
Transcription Initiation ◽  
Xeroderma Pigmentosum ◽  
Initiation Site ◽  
Specific Protein ◽  
Complementation Group ◽  
Cross Linking ◽  
Promoter Melting ◽  
Group B

ABSTRACT The p89/xeroderma pigmentosum complementation group B (XPB) ATPase-helicase of transcription factor IIH (TFIIH) is essential for promoter melting prior to transcription initiation by RNA polymerase II (RNAPII). By studying the topological organization of the initiation complex using site-specific protein-DNA photo-cross-linking, we have shown that p89/XPB makes promoter contacts both upstream and downstream of the initiation site. The upstream contact, which is in the region where promoter melting occurs (positions −9 to +2), requires tight DNA wrapping around RNAPII. The addition of hydrolyzable ATP tethers the template strand at positions −5 and +1 to RNAPII subunits. A mutation in p89/XPB found in a xeroderma pigmentosum patient impairs the ability of TFIIH to associate correctly with the complex and thereby melt promoter DNA. A model for open complex formation is proposed.

scholarly journals Transcription-Associated Breaks in Xeroderma Pigmentosum Group D Cells from Patients with Combined Features of Xeroderma Pigmentosum and Cockayne Syndrome

2005 ◽  
Vol 25 (18) ◽  
pp. 8368-8378 ◽  
Author(s):  
Therina Theron ◽  
Maria I. Fousteri ◽  
Marcel Volker ◽  
Lorna W. Harries ◽  
Elena Botta ◽  
...  
Keyword(s):  
Rna Polymerase ◽  
Rna Polymerase Ii ◽  
Transcription Initiation ◽  
Xeroderma Pigmentosum ◽  
Excision Repair ◽  
Cockayne Syndrome ◽  
Combined Features ◽  
D Cells ◽  
Cellular Dna ◽  
Carboxy Terminal

ABSTRACT Defects in the XPD gene can result in several clinical phenotypes, including xeroderma pigmentosum (XP), trichothiodystrophy, and, less frequently, the combined phenotype of XP and Cockayne syndrome (XP-D/CS). We previously showed that in cells from two XP-D/CS patients, breaks were introduced into cellular DNA on exposure to UV damage, but these breaks were not at the sites of the damage. In the present work, we show that three further XP-D/CS patients show the same peculiar breakage phenomenon. We show that these breaks can be visualized inside the cells by immunofluorescence using antibodies to either γ-H2AX or poly-ADP-ribose and that they can be generated by the introduction of plasmids harboring methylation or oxidative damage as well as by UV photoproducts. Inhibition of RNA polymerase II transcription by four different inhibitors dramatically reduced the number of UV-induced breaks. Furthermore, the breaks were dependent on the nucleotide excision repair (NER) machinery. These data are consistent with our hypothesis that the NER machinery introduces the breaks at sites of transcription initiation. During transcription in UV-irradiated XP-D/CS cells, phosphorylation of the carboxy-terminal domain of RNA polymerase II occurred normally, but the elongating form of the polymerase remained blocked at lesions and was eventually degraded.

scholarly journals Reduced RNA polymerase II transcription in intact and permeabilized Cockayne syndrome group B cells

1997 ◽  
Vol 94 (9) ◽  
pp. 4306-4311 ◽  
Author(s):  
A. S. Balajee ◽  
A. May ◽  
G. L. Dianov ◽  
E. C. Friedberg ◽  
V. A. Bohr
Keyword(s):  
B Cells ◽  
Rna Polymerase ◽  
Rna Polymerase Ii ◽  
Cockayne Syndrome ◽  
Group B ◽  
Rna Polymerase Ii Transcription

scholarly journals Evidence that the Transcription Elongation Function of Rpb9 Is Involved in Transcription-Coupled DNA Repair in Saccharomyces cerevisiae

2006 ◽  
Vol 26 (24) ◽  
pp. 9430-9441 ◽  
Author(s):  
Shisheng Li ◽  
Baojin Ding ◽  
Runqiang Chen ◽  
Christine Ruggiero ◽  
Xuefeng Chen
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Dna Repair ◽  
Rna Polymerase ◽  
Rna Polymerase Ii ◽  
Transcription Elongation ◽  
Elongation Factor ◽  
Complementation Group ◽  
Cockayne Syndrome ◽  
Transcription Repression ◽  
Group B

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.

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