Elaine O. Davis

Journal Article Protein splicing elements: inteins and exteins — a definition of terms and recommended nomenclature Get access Francine B. Perler, Francine B. Perler * *To whom correspondence should be addressed Search for other works by this author on: Oxford Academic PubMed Google Scholar Elaine O. Davis, Elaine O. Davis 1National Institute for Medical ResearchMill Hill, London, UK Search for other works by this author on: Oxford Academic PubMed Google Scholar Gary E. Dean, Gary E. Dean 2University of Cincinnati College of MedicineCincinnati, OH 45267-0524 Search for other works by this author on: Oxford Academic PubMed Google Scholar Frederick S. Gimble, Frederick S. Gimble 3Institute of Biosciences and Technology, Texas A & M UniversityHouston, TX 77030-3303 Search for other works by this author on: Oxford Academic PubMed Google Scholar William E. Jack, William E. Jack Search for other works by this author on: Oxford Academic PubMed Google Scholar Norma Neff, Norma Neff 4Sloan-Kettering, Molecular Biology ProgramNew York, NY 10021 Search for other works by this author on: Oxford Academic PubMed Google Scholar Christopher J. Noren, Christopher J. Noren Search for other works by this author on: Oxford Academic PubMed Google Scholar Jeremy Thorner, Jeremy Thorner 5University of CaliforniaBerkeley, CA 94720 Search for other works by this author on: Oxford Academic PubMed Google Scholar Marlene Belfort Marlene Belfort 6Wadsworth Center for Laboratories and Research, NY State Department of HealthAlbany, NY 12201-0509, USA Search for other works by this author on: Oxford Academic PubMed Google Scholar Nucleic Acids Research, Volume 22, Issue 7, 11 April 1994, Pages 1125–1127, https://doi.org/10.1093/nar/22.7.1125 Published: 11 April 1994 Article history Received: 24 November 1993 Revision received: 28 February 1994 Accepted: 28 February 1994 Published: 11 April 1994

In many species of bacteria most inducible DNA repair genes are regulated by LexA homologues and are dependent on RecA for induction. We have shown previously by analysing the induction of recA that two mechanisms for the induction of gene expression following DNA damage exist in Mycobacterium tuberculosis. Whereas one of these depends on RecA and LexA in the classical way, the other mechanism is independent of both of these proteins and induction occurs in the absence of RecA. Here we investigate the generality of each of these mechanisms by analysing the global response to DNA damage in both wild-type M. tuberculosis and a recA deletion strain of M. tuberculosis using microarrays. This revealed that the majority of the genes that were induced remained inducible in the recA mutant stain. Of particular note most of the inducible genes with known or predicted functions in DNA repair did not depend on recA for induction. Amongst these are genes involved in nucleotide excision repair, base excision repair, damage reversal and recombination. Thus, it appears that this novel mechanism of gene regulation is important for DNA repair in M. tuberculosis.