Prophage induction and differential RecA and UmuDAb transcriptome regulation in the DNA damage responses of Acinetobacter baumannii and Acinetobacter baylyi.
The SOS response to DNA damage that induces up to 10% of the prokaryotic genome requires RecA action to relieve LexA transcriptional repression. In Acinetobacter species, which lack LexA, the error-prone polymerase accessory UmuDAb is instead required for ddrR induction after DNA damage, suggesting it might be a LexA analog. RNA-Seq experiments defined the DNA damage transcriptome (mitomycin C-induced) of wild type, recA and umuDAb mutant strains of both A. baylyi ADP1 and A. baumannii ATCC 17978. Of the typical SOS response genes, few were differentially regulated in these species; many were repressed or absent. A striking 38.4% of all ADP1 genes, and 11.4% of all 17978 genes, were repressed under these conditions. In A. baylyi ADP1, 66 genes (2.0% of the genome), including a CRISPR/Cas system, were DNA damage-induced, and belonged to four regulons defined by differential use of recA and umuDAb. In A. baumannii ATCC 17978, however, induction of 99% of the 152 mitomycin C-induced genes depended on recA, and only 28 of these genes required umuDAb for their induction. 90% of the induced A. baumannii genes were clustered in three prophage regions, and bacteriophage particles were observed after mitomycin C treatment. These prophages encoded esvI, esvK1, and esvK2, ethanol-stimulated virulence genes previously identified in a Caenorhabditis elegans model, as well as error-prone polymerase alleles. The induction of all 17978 error-prone polymerase alleles, whether prophage-encoded or not, was recA dependent, but only these DNA polymerase V-related genes were de-repressed in the umuDAb mutant in the absence of DNA damage. These results suggest that both species possess a robust and complex DNA damage response involving both recA-dependent and recA-independent regulons, and further demonstrates that although umuDAb has a specialized role in repressing error-prone polymerases, additional regulators likely participate in these species' transcriptional response to DNA damage.
Department of Biology and Chemistry, Morehead State University, Morehead, Kentucky, United States of America.
Janelle M
JM
Hare
Department of Biology and Chemistry, Morehead State University, Morehead, Kentucky, United States of America.
Joshua C
JC
Ferrell
Department of Biology and Chemistry, Morehead State University, Morehead, Kentucky, United States of America.
Travis A
TA
Witkowski
Department of Biology and Chemistry, Morehead State University, Morehead, Kentucky, United States of America.
Alison N
AN
Grice
D000150:Acinetobacter / Q000235:genetics*; D040981:Acinetobacter baumannii / Q000235:genetics*; D001426:Bacterial Proteins / Q000235:genetics* / Q000378:metabolism; D004249:DNA Damage / Q000187:drug effects / Q000235:genetics*; D004268:DNA-Binding Proteins / Q000235:genetics* / Q000378:metabolism; D015964:Gene Expression Regulation, Bacterial / Q000187:drug effects / Q000235:genetics*; D016685:Mitomycin / Q000494:pharmacology; D011938:Rec A Recombinases / Q000235:genetics* / Q000378:metabolism; D059467:Transcriptome / Q000187:drug effects / Q000235:genetics*; D014775:Virus Activation / Q000187:drug effects / Q000235:genetics*
D001426:Bacterial Proteins; D004268:DNA-Binding Proteins; C089760:RecA protein, Acinetobacter calcoaceticus; D016685:Mitomycin; D011938:Rec A Recombinases