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Activation and modulation of the host response to DNA damage by an integrative and conjugative element
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Abstract
Mobile genetic elements help drive horizontal gene transfer and bacterial evolution. Conjugative elements and temperate bacteriophages can be stably maintained in host cells. They can alter host physiology and regulatory responses and typically carry genes that are beneficial to their hosts. We found that ICE
Bs1
, an integrative and conjugative element of
Bacillus subtilis
, inhibits the host response to DNA damage (the SOS response). Activation of ICE
Bs1
before DNA damage reduced host cell lysis that was caused by SOS-mediated activation of two resident prophages. Further, activation of ICE
Bs1
itself activated the SOS response in a subpopulation of cells, and this activation was attenuated by the functions of the ICE
Bs1
genes
ydcT
and
yddA
(now
ramT
and
ramA
, for RecA modulator). Double mutant analyses indicated that RamA functions to inhibit and RamT functions to both inhibit and activate the SOS response. Both RamT and RamA caused a reduction in RecA filaments, one of the early steps in activation of the SOS response. We suspect that there are several different mechanisms by which mobile genetic elements that generate ssDNA during their lifecycle inhibit the host SOS response and RecA function, as RamT and RamA differ from the known SOS inhibitors encoded by conjugative elements.
Title: Activation and modulation of the host response to DNA damage by an integrative and conjugative element
Description:
Abstract
Mobile genetic elements help drive horizontal gene transfer and bacterial evolution.
Conjugative elements and temperate bacteriophages can be stably maintained in host cells.
They can alter host physiology and regulatory responses and typically carry genes that are beneficial to their hosts.
We found that ICE
Bs1
, an integrative and conjugative element of
Bacillus subtilis
, inhibits the host response to DNA damage (the SOS response).
Activation of ICE
Bs1
before DNA damage reduced host cell lysis that was caused by SOS-mediated activation of two resident prophages.
Further, activation of ICE
Bs1
itself activated the SOS response in a subpopulation of cells, and this activation was attenuated by the functions of the ICE
Bs1
genes
ydcT
and
yddA
(now
ramT
and
ramA
, for RecA modulator).
Double mutant analyses indicated that RamA functions to inhibit and RamT functions to both inhibit and activate the SOS response.
Both RamT and RamA caused a reduction in RecA filaments, one of the early steps in activation of the SOS response.
We suspect that there are several different mechanisms by which mobile genetic elements that generate ssDNA during their lifecycle inhibit the host SOS response and RecA function, as RamT and RamA differ from the known SOS inhibitors encoded by conjugative elements.
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