Control of methionine metabolism by the SahR transcriptional regulator in P roteobacteria
Sulphur is an essential element in the metabolism. The sulphur‐containing amino acid methionine is a metabolic precursor for S ‐adenosylmethionine ( SAM ), which serves as a coenzyme for ubiquitous methyltrtansferases. Recycling of organic sulphur compounds, e.g. via the SAM cycle, is an important m...
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Veröffentlicht in: | Environmental microbiology 2014-01, Vol.16 (1), p.1-8 |
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Sprache: | eng |
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Zusammenfassung: | Sulphur is an essential element in the metabolism. The sulphur‐containing amino acid methionine is a metabolic precursor for
S
‐adenosylmethionine (
SAM
), which serves as a coenzyme for ubiquitous methyltrtansferases. Recycling of organic sulphur compounds, e.g. via the
SAM
cycle, is an important metabolic process that needs to be tightly regulated. Knowledge about transcriptional regulation of these processes is still limited for many free‐living bacteria. We identified a novel transcription factor
SahR
from the
ArsR
family that controls the
SAM
cycle genes in diverse microorganisms from soil and aquatic ecosystems. By using comparative genomics, we predicted
SahR
‐binding
DNA
motifs and reconstructed
SahR
regulons in the genomes of 62
P
roteobacteria. The conserved core of
SahR
regulons includes all enzymes required for the
SAM
cycle: the
SAH
hydrolase
AhcY
, the methionine biosynthesis enzymes
MetE
/
MetH
and
MetF
, and the
SAM
synthetase
MetK
. By using a combination of experimental techniques, we validated the
SahR
regulon in the sulphate‐reducing
D
eltaproteobacterium
D
esulfovibrio alaskensis
.
SahR
functions as a negative regulator that responds to the
S
‐adenosylhomocysteine (
SAH
). The elevated
SAH
level in the cell dissociates
SahR
from its
DNA
operators and induces the expression of
SAM
cycle genes. The effector‐sensing domain in
SahR
is related to
SAM
‐dependent methylases that are able to tightly bind
SAH
.
SahR
represents a novel type of transcriptional regulators for the control of sulphur amino acid metabolism. |
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ISSN: | 1462-2912 1462-2920 |
DOI: | 10.1111/1462-2920.12273 |