The global regulator GacS of a biocontrol bacterium Pseudomonas chlororaphis O6 regulates transcription from the rpoS gene encoding a stationary-phase sigma factor and affects survival in oxidative stress
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作者:
Kang, BR
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机构:Chonnam Natl Univ, Agr Plant Stress Res Ctr, Kwangju 500757, South Korea
Kang, BR
Chou, BH
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机构:Chonnam Natl Univ, Agr Plant Stress Res Ctr, Kwangju 500757, South Korea
Chou, BH
Anne, AJ
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机构:Chonnam Natl Univ, Agr Plant Stress Res Ctr, Kwangju 500757, South Korea
Anne, AJ
Kim, YC
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Chonnam Natl Univ, Agr Plant Stress Res Ctr, Kwangju 500757, South KoreaChonnam Natl Univ, Agr Plant Stress Res Ctr, Kwangju 500757, South Korea
Kim, YC
[1
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[1] Chonnam Natl Univ, Agr Plant Stress Res Ctr, Kwangju 500757, South Korea
[2] Chonnam Natl Univ, Coll Agr & Life Sci, Inst Agr Sci & Technol, Kwangju 500757, South Korea
[3] Utah State Univ, Dept Biol, Logan, UT 84322 USA
The global regulator, GacS (global activator for antibiotics and cyanide sensor kinase), of the rbizosphere bacterium Pseudomonas chlororaphis O6 (Pc O6) was required for increased resistance to hydrogen peroxide as cultures mature. Specific bands of peroxidase and catalase activity were absent in the stationary-phase cells of the Pc O6 gacS mutant, whereas a manganese superoxide dismutase (MnSOD) isozyme was expressed earlier and to a greater extent than in the wild-type. In the wild-type cell, transcript accumulation of rpoS was higher in late logarithmic (log)-phase cells than cells from mid log-phase or stationary-phase. Transcript abundance from rpoS was reduced in the gacS mutant throughout the growth phase compared to the wild-type expression. The sequence of a small RNA, rsmZ, found downstream of rpoS in other pseudomonads was lacking in Pe O6. This RNA is implicated in the control of genes activated by the GacS system. Thus, the mechanism by which GacS mediates the activation of genes under its control requires further investigation in Pc O6. (C) 2003 Elsevier B.V. All rights reserved.
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Penn State Univ, Dept Biol, Mueller Lab 208, Inst Mol Evolut Genet, University Pk, PA 16802 USAPenn State Univ, Dept Biol, Mueller Lab 208, Inst Mol Evolut Genet, University Pk, PA 16802 USA
Herbelin, CJ
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Chirillo, SC
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Penn State Univ, Dept Biol, Mueller Lab 208, Inst Mol Evolut Genet, University Pk, PA 16802 USAPenn State Univ, Dept Biol, Mueller Lab 208, Inst Mol Evolut Genet, University Pk, PA 16802 USA
Chirillo, SC
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Melnick, KA
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Penn State Univ, Dept Biol, Mueller Lab 208, Inst Mol Evolut Genet, University Pk, PA 16802 USAPenn State Univ, Dept Biol, Mueller Lab 208, Inst Mol Evolut Genet, University Pk, PA 16802 USA
Melnick, KA
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Whittam, TS
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Penn State Univ, Dept Biol, Mueller Lab 208, Inst Mol Evolut Genet, University Pk, PA 16802 USAPenn State Univ, Dept Biol, Mueller Lab 208, Inst Mol Evolut Genet, University Pk, PA 16802 USA
机构:
Penn State Univ, Dept Biol, Mueller Lab 208, Inst Mol Evolut Genet, University Pk, PA 16802 USAPenn State Univ, Dept Biol, Mueller Lab 208, Inst Mol Evolut Genet, University Pk, PA 16802 USA
Herbelin, CJ
;
Chirillo, SC
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Penn State Univ, Dept Biol, Mueller Lab 208, Inst Mol Evolut Genet, University Pk, PA 16802 USAPenn State Univ, Dept Biol, Mueller Lab 208, Inst Mol Evolut Genet, University Pk, PA 16802 USA
Chirillo, SC
;
Melnick, KA
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Penn State Univ, Dept Biol, Mueller Lab 208, Inst Mol Evolut Genet, University Pk, PA 16802 USAPenn State Univ, Dept Biol, Mueller Lab 208, Inst Mol Evolut Genet, University Pk, PA 16802 USA
Melnick, KA
;
Whittam, TS
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Penn State Univ, Dept Biol, Mueller Lab 208, Inst Mol Evolut Genet, University Pk, PA 16802 USAPenn State Univ, Dept Biol, Mueller Lab 208, Inst Mol Evolut Genet, University Pk, PA 16802 USA