Authors
Poteete, Anthony R.UMass Chan Affiliations
Department of Microbiology and Physiological SystemsDocument Type
Journal ArticlePublication Date
2011-03-31Keywords
Escherichia coliEscherichia coli Proteins
*Mutation
Phenotype
Rec A Recombinases
*Recombination, Genetic
Transcription Factors
Biochemistry, Biophysics, and Structural Biology
Life Sciences
Medicine and Health Sciences
Metadata
Show full item recordAbstract
BACKGROUND: The elongation factor GreA binds to RNA polymerase and modulates transcriptional pausing. Some recent research suggests that the primary role of GreA may not be to regulate gene expression, but rather, to promote the progression of replication forks which collide with RNA polymerase, and which might otherwise collapse. Replication fork collapse is known to generate dsDNA breaks, which can be recombinogenic. It follows that GreA malfunction could have consequences affecting homologous recombination. RESULTS: Escherichia coli mutants bearing substitutions of the active site acidic residues of the transcription elongation factor GreA, D41N and E44K, were isolated as suppressors of growth inhibition by a toxic variant of the bacteriophage lambda Red-beta recombination protein. These mutants, as well as a D41A greA mutant and a greA deletion, were tested for proficiency in recombination events. The mutations were found to increase the efficiency of RecA-RecBCD-mediated and RecA-Red-mediated recombination, which are replication-independent, and to decrease the efficiency of replication-dependent Red-mediated recombination. CONCLUSION: These observations provide new evidence for a role of GreA in resolving conflicts between replication and transcription.Source
BMC Mol Biol. 2011 Mar 31;12:12. Link to article on publisher's siteDOI
10.1186/1471-2199-12-12Permanent Link to this Item
http://hdl.handle.net/20.500.14038/39488PubMed ID
21453489; 21453489Related Resources
Link to Article in PubMedRights
© 2011 Poteete; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
ae974a485f413a2113503eed53cd6c53
10.1186/1471-2199-12-12