An epigenetic switch activates bacterial quorum sensing and horizontal transfer of an integrative and conjugative element

An epigenetic switch activates bacterial quorum sensing and horizontal transfer of an integrative and conjugative element

Horizontal transfer of the integrative and conjugative element ICEMlSymR7A converts non-symbiotic Mesorhizobium spp. into nitrogen-fixing legume symbionts. Here, we discover subpopulations of Mesorhizobium japonicum R7A become epigenetically primed for quorum-sensing (QS) and QS-activated horizontal...

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Bibliographic Details
Main Authors: Ramsay, Josh, Bastholm, T.R., Verdonk, Callum J., Tambalo, D.D., Sullivan, J.T., Harold, L.K., Panganiban, Beatrice A., Colombi, Elena, Perry, B.J., Jowsey, W., Morris, C., Hynes, M.F., Bond, C.S., Cameron, A.D.S., Yost, C.K., Ronson, C.W.
Format: Journal Article
Language:English
Published: OXFORD UNIV PRESS 2022
Subjects:
Science & Technology
Life Sciences & Biomedicine
Biochemistry & Molecular Biology
SYMBIOSIS ISLAND
MESORHIZOBIUM-LOTI
TRANSCRIPTION REGULATION
BACILLUS-SUBTILIS
GENE
PLASMID
BISTABILITY
EXPRESSION
EVOLUTION
PROTEIN
Online Access:http://purl.org/au-research/grants/arc/FT170100235
http://hdl.handle.net/20.500.11937/89033
Description
Summary:Horizontal transfer of the integrative and conjugative element ICEMlSymR7A converts non-symbiotic Mesorhizobium spp. into nitrogen-fixing legume symbionts. Here, we discover subpopulations of Mesorhizobium japonicum R7A become epigenetically primed for quorum-sensing (QS) and QS-activated horizontal transfer. Isolated populations in this state termed R7A* maintained these phenotypes in laboratory culture but did not transfer the R7A* state to recipients of ICEMlSymR7A following conjugation. We previously demonstrated ICEMlSymR7A transfer and QS are repressed by the antiactivator QseM in R7A populations and that the adjacently-coded DNA-binding protein QseC represses qseM transcription. Here RNA-sequencing revealed qseM expression was repressed in R7A* cells and that RNA antisense to qseC was abundant in R7A but not R7A*. Deletion of the antisense-qseC promoter converted cells into an R7A*-like state. An adjacently coded QseC2 protein bound two operator sites and repressed antisense-qseC transcription. Plasmid overexpression of QseC2 stimulated the R7A* state, which persisted following curing of this plasmid. The epigenetic maintenance of the R7A* state required ICEMlSymR7A-encoded copies of both qseC and qseC2. Therefore, QseC and QseC2, together with their DNA-binding sites and overlapping promoters, form a stable epigenetic switch that establishes binary control over qseM transcription and primes a subpopulation of R7A cells for QS and horizontal transfer.

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