Nucleic Acids Research, 2001, Vol. 29, No. 9 1884-1891
© 2001 Oxford University Press
Cloning the human and mouse MMS19 genes and functional complementation of a yeast mms19 deletion mutant
1Laboratory of Molecular Pathology, Department of Pathology and 2Genome Science and Technology Center, University of Texas Southwestern Medical Center, Dallas, TX 75390-9072, USA, 3National Center for Biotechnology Information, National Library of Medicine, National Institutes of Health, Bethesda, MD 20894,USA, 4Department of Biology, Texas A & M University, College Station, TX 70843, USA and 5Istituto di Genetica Biochimica ed Evoluzionistica, 27100 Pavia, Italy
The MMS19 gene of the yeast Saccharomyces cerevisiae encodes a polypeptide of unknown function which is required for both nucleotide excision repair (NER) and RNA polymerase II (RNAP II) transcription. Here we report the molecular cloning of human and mouse orthologs of the yeast MMS19 gene. Both human and Drosophila MMS19 cDNAs correct thermosensitive growth and sensitivity to killing by UV radiation in a yeast mutant deleted for the MMS19 gene, indicating functional conservation between the yeast and mammalian gene products. Alignment of the translated sequences of MMS19 from multiple eukaryotes, including mouse and human, revealed the presence of several conserved regions, including a HEAT repeat domain near the C-terminus. The presence of HEAT repeats, coupled with functional complementation of yeast mutant phenotypes by the orthologous protein from higher eukaryotes, suggests a role of Mms19 protein in the assembly of a multiprotein complex(es) required for NER and RNAP II transcription. Both the mouse and human genes are ubiquitously expressed as multiple transcripts, some of which appear to derive from alternative splicing. The ratio of different transcripts varies in several different tissue types.
* To whom correspondence should be addressed at: Department of Pathology, Room NB6.212A, University of Texas Southwestern Medical Center, 6000 Harry Hines Boulevard, Dallas, TX 75390-9072, USA. Tel: +1 214 648 4020; Fax: +1 214 648 4067; Email: friedberg.errol{at}pathology.swmed.edu
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  R. R. McWilliams, W. R. Bamlet, M. de Andrade, D. N. Rider, J. M. Cunningham, and G. M. Petersen Nucleotide Excision Repair Pathway Polymorphisms and Pancreatic Cancer Risk: Evidence for role of MMS19L Cancer Epidemiol. Biomarkers Prev., April 1, 2009; 18(4): 1295 - 1302. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. Kou, Y. Zhou, R. M. C. Gorospe, and Z. Wang Mms19 protein functions in nucleotide excision repair by sustaining an adequate cellular concentration of the TFIIH component Rad3 PNAS, October 14, 2008; 105(41): 15714 - 15719. [Abstract] [Full Text] [PDF]
|
|