Analysis of LexA binding sites and transcriptomics in response to genotoxic stress in Leptospira interrogans
Name
Schons-Fonseca-2016-Analysis of LexA bin.pdf
Size
10.02 MB
Format
Adobe PDF
Checksum (MD5)
f79d4030d20284be3d970cc012d359b4
Author(s)
Schons-Fonseca, Luciane
da Silva, Josefa B.
Milanez, Juliana S.
Domingos, Renan H.
Smith, Janet L.
Nakaya, Helder I.
Ho, Paulo L.
da Costa, Renata MA
Grossman, Alan Davis
Date Issued
February 2016
Journal
Nucleic Acids Research
Publisher
Oxford University Press
Citation
Schons-Fonseca, Luciane, Josefa B. da Silva, Juliana S. Milanez, Renan H. Domingos, Janet L. Smith, Helder I. Nakaya, Alan D. Grossman, Paulo L. Ho, and Renata MA da Costa. “Analysis of LexA Binding Sites and Transcriptomics in Response to Genotoxic Stress in Leptospira Interrogans.” Nucleic Acids Research 44, no. 3 (January 13, 2016): 1179–1191.
Version
Final published version
Abstract
We determined the effects of DNA damage caused by ultraviolet radiation on gene expression in Leptospira interrogans using DNA microarrays. These data were integrated with DNA binding in vivo of LexA1, a regulator of the DNA damage response, assessed by chromatin immunoprecipitation and massively parallel DNA sequencing (ChIP-seq). In response to DNA damage, Leptospira induced expression of genes involved in DNA metabolism, in mobile genetic elements and defective prophages. The DNA repair genes involved in removal of photo-damage (e.g. nucleotide excision repair uvrABC, recombinases recBCD and resolvases ruvABC) were not induced. Genes involved in various metabolic pathways were down regulated, including genes involved in cell growth, RNA metabolism and the tricarboxylic acid cycle. From ChIP-seq data, we observed 24 LexA1 binding sites located throughout chromosome 1 and one binding site in chromosome 2. Expression of many, but not all, genes near those sites was increased following DNA damage. Binding sites were found as far as 550 bp upstream from the start codon, or 1 kb into the coding sequence. Our findings indicate that there is a shift in gene expression following DNA damage that represses genes involved in cell growth and virulence, and induces genes involved in mutagenesis and recombination.
MIT Department
Massachusetts Institute of Technology. Department of Biology
Terms of Use
Creative Commons Attribution
Persistent DSpace Link
DOI of Published Version
https://doi.org/10.1093/nar/gkv1536
