Pleiotropic Effect of Salt Stress on Motility and Synthesis of Secreted Ribonucleases by Bacillus pumilus

Members of the genus Bacillus can successfully counteract a sudden increase in salinity. In addition to the accumulation of osmolytes, saline stress also affects other aspects of bacterial physiology such as exoenzymes synthesis and motility. Here, we have shown that increase of salinity in growth m...

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Bibliographic Details
Published in:BioNanoScience 2017-12, Vol.7 (4), p.623-626
Main Authors: Kharitonova, M.A., Evtugyn, V.G., Kolpakov, A.I.
Format: Article
Language:English
Subjects:
Abiotic stress
Bacillus pumilus
Bacteria
Biological and Medical Physics
Biomaterials
Biophysics
Biosynthesis
Circuits and Systems
Electron microscopy
Engineering
Flagella
Gene sequencing
Homology
Lymphocytes B
Molecular weight
Motility
Mutation
Nanotechnology
Ribonuclease
Salinity
Salinity effects
Signal transduction
Stresses
Transduction
Transmission electron microscopy
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Summary:Members of the genus Bacillus can successfully counteract a sudden increase in salinity. In addition to the accumulation of osmolytes, saline stress also affects other aspects of bacterial physiology such as exoenzymes synthesis and motility. Here, we have shown that increase of salinity in growth medium leads to elevated biosynthesis level of low-molecular weight ribonuclease (RNase) binase I from Bacillus pumilus . The same effect was established previously for high-molecular weight binase II. Transmission electron microscopy revealed the absence of flagella and some other changes in salt-stressed cells of B. pumilis . We also detected the gene sequences homologous to the recognition sites of response regulator DegU in the binase I and binase II promoters. Using the B. subtilis strains with various mutations in DegU gene, we found that the two-component signal transduction system DegS-DegU which regulates the motility under salt stress participates in the control of biosynthesis for both secreted RNase of B. pumilis (binase I and binase II).
ISSN:2191-1630
2191-1649
DOI:10.1007/s12668-017-0460-9