This study provides the first evidence for the extensive control
that salt stress exerts on iron homeostasis in the halophilic
bacterium and ectoine producer C. salexigens. The extent of
this control is such that in salt-stressed C. salexigens there is a
lower requirement for iron and, concomitantly, siderophore
synthesis is repressed. These processes are controlled by the
global regulator Fur, the first iron uptake regulator characterized
in a moderately halophilic bacterium, which also functions
as a positive regulator of ectoine synthesis at high salinity,
linking the osmostress response to iron homeostasis in this
halophilic microorganism.
In B. subtilis members of the Fur regulon were induced by
high salinity, suggesting that cells grown under osmotic stress
conditions experienced severe iron limitation. In support of
this suggestion, addition of excess iron to cells grown with high
salt partially reversed the growth defect exhibited by saltstressed
B. subtilis cultures and reduced the high-salinity-mediated
induction of many of the Fur-regulated genes (37, 69).
We observed the opposite effect in C. salexigens; that is, greater
osmotic stress was correlated with a lower demand for iron.
The reason(s) for this difference is unknown. However, the two
organisms have different ranges of salinity for growth, and the
salinity referred in B. subtilis studies as “high” was 0.7 M NaCl,
which corresponded approximately to the “low” salinity in our
study. In addition, the B. subtilis strain for which the effect of
salinity on iron demand was observed contains a mutation
(sfp0
) that prevents or strongly reduces the synthesis of the
main siderophore, bacillibactin. However, when the B. subtilis
wild-type strain was used, an increase in the salinity of the
growth medium had only a marginal effect on the synthesis of
2,3-dihydroxybenzoate, the bacillibactin precursor. Moreover,
high-salinity-mediated growth retardation of the wild type
could not be rescued increasing the iron concentration of the
growth medium (37). Therefore, the wild-type B. subtilis strain
did not exhibit the iron limitation observed in the mutant strain
whose siderophore synthesis was affected at high salinity.
This study provides the first evidence for the extensive controlthat salt stress exerts on iron homeostasis in the halophilicbacterium and ectoine producer C. salexigens. The extent ofthis control is such that in salt-stressed C. salexigens there is alower requirement for iron and, concomitantly, siderophoresynthesis is repressed. These processes are controlled by theglobal regulator Fur, the first iron uptake regulator characterizedin a moderately halophilic bacterium, which also functionsas a positive regulator of ectoine synthesis at high salinity,linking the osmostress response to iron homeostasis in thishalophilic microorganism.In B. subtilis members of the Fur regulon were induced byhigh salinity, suggesting that cells grown under osmotic stressconditions experienced severe iron limitation. In support ofthis suggestion, addition of excess iron to cells grown with highsalt partially reversed the growth defect exhibited by saltstressedB. subtilis cultures and reduced the high-salinity-mediatedinduction of many of the Fur-regulated genes (37, 69).We observed the opposite effect in C. salexigens; that is, greaterosmotic stress was correlated with a lower demand for iron.The reason(s) for this difference is unknown. However, the twoorganisms have different ranges of salinity for growth, and thesalinity referred in B. subtilis studies as “high” was 0.7 M NaCl,which corresponded approximately to the “low” salinity in ourstudy. In addition, the B. subtilis strain for which the effect ofsalinity on iron demand was observed contains a mutation(sfp0) that prevents or strongly reduces the synthesis of themain siderophore, bacillibactin. However, when the B. subtiliswild-type strain was used, an increase in the salinity of thegrowth medium had only a marginal effect on the synthesis of2,3-dihydroxybenzoate, the bacillibactin precursor. Moreover,high-salinity-mediated growth retardation of the wild typecould not be rescued increasing the iron concentration of thegrowth medium (37). Therefore, the wild-type B. subtilis straindid not exhibit the iron limitation observed in the mutant strainwhose siderophore synthesis was affected at high salinity.
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