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Diguanylate cyclase NicD ‐based signalling mechanism of nutrient‐induced dispersion by P seudomonas aeruginosa
Dispersion enables the transition from the biofilm to the planktonic growth state in response to various cues. While several P seudomonas aeruginosa proteins, including BdlA and the c‐di‐ GMP phosphodiesterases DipA , RbdA , and NbdA , have been shown to be required for dispersion to occur, little i...
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Published in: | Molecular microbiology 2014-11, Vol.94 (4), p.771-793 |
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Main Authors: | , |
Format: | Article |
Language: | English |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Dispersion enables the transition from the biofilm to the planktonic growth state in response to various cues. While several
P
seudomonas aeruginosa
proteins, including
BdlA
and the c‐di‐
GMP
phosphodiesterases
DipA
,
RbdA
, and
NbdA
, have been shown to be required for dispersion to occur, little is known about dispersion cue sensing and the signalling translating these cues into the modulation c‐di‐
GMP
levels to enable dispersion. Using glutamate‐induced dispersion as a model, we report that dispersion‐inducing nutrient cues are sensed via an outside‐in signalling mechanism by the diguanylate cyclase
NicD
belonging to a family of seven transmembrane (7
TM
) receptors.
NicD
directly interacts with
BdlA
and the phosphodiesterase
DipA
, with
NicD
,
BdlA
, and
DipA
being part of the same pathway required for dispersion. Glutamate sensing by
NicD
results in
NicD
dephosphorylation and increased cyclase activity. Active
NicD
contributes to the non‐processive proteolysis and activation of
BdlA
via phosphorylation and temporarily elevated c‐di‐
GMP
levels.
BdlA
, in turn, activates
DipA
, resulting in the overall reduction of c‐di‐
GMP
levels. Our results provide a basis for understanding the signalling mechanism based on
NicD
to induce biofilm dispersion that may be applicable to various biofilm‐forming species and may have implications for the control of biofilm‐related infections. |
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ISSN: | 0950-382X 1365-2958 |
DOI: | 10.1111/mmi.12802 |