The histidine kinase Hik33 perceives osmotic stress and cold stress in Synechocystis sp. PCC 6803

Authors

  • Koji Mikami,

    1. Department of Regulation Biology, National Institute for Basic Biology, Okazaki, Japan.
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  • Yu Kanesaki,

    1. Department of Regulation Biology, National Institute for Basic Biology, Okazaki, Japan.
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  • Iwane Suzuki,

    1. Department of Regulation Biology, National Institute for Basic Biology, Okazaki, Japan.
    2. Department of Molecular Biomechanics, Graduate University for Advanced Studies, Okazaki, Japan.
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  • Norio Murata

    Corresponding author
    1. Department of Regulation Biology, National Institute for Basic Biology, Okazaki, Japan.
    2. Department of Molecular Biomechanics, Graduate University for Advanced Studies, Okazaki, Japan.
    • For correspondence. E-mail murata@ nibb.ac.jp ; Tel. (+81) 564 55 7600; Fax (+81) 564 54 4866.

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Summary

The stress imposed on living organisms by hyperosmotic conditions and low temperature appears to be perceived via changes in the physical state of membrane lipids. We compared genome-wide patterns of transcription between wild-type Synechocystis sp. PCC 6803 and cells with a mutation in the histidine kinase Hik33 using a DNA microarray. Our results indicated that Hik33 regulated the expression of both osmostress-inducible and cold-inducible genes. The respective genes that were regulated by Hik33 under hyperosmotic and low-temperature conditions were, for the most part, different from one another. However, Hik33 also regulated the expression of a set of genes whose expression was induced both by osmotic stress and by cold stress. These results indicate that Hik33 is involved in responses to osmotic stress and low-temperature stress but that the mechanisms of the responses differ.

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