An Arabidopsis R2R3-MYB transcription factor, AtMYB20, negatively regulates type 2C serine/threonine protein phosphatases to enhance salt tolerance

•AtMYB20-OX showed enhanced while AtMYB20-SRDX showed reduced salt stress tolerance.•PP2Cs were suppressed in AtMYB20-OX and enhanced in AtMYB20-SRDX by NaCl treatment.•AtMYB20 binds to the ABI1 promoter region containing a MYB recognition element in vitro.•AtMYB20 binds to the ABI1 and AtPP2CA prom...

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Veröffentlicht in:FEBS letters 2013-06, Vol.587 (12), p.1773-1778
Hauptverfasser: Cui, Mei Hua, Yoo, Kyoung Shin, Hyoung, Sujin, Nguyen, Ha Thi Kim, Kim, Yun Young, Kim, Hae Jin, Ok, Sung Han, Yoo, Sang Dong, Shin, Jeong Sheop
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Sprache:eng
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Zusammenfassung:•AtMYB20-OX showed enhanced while AtMYB20-SRDX showed reduced salt stress tolerance.•PP2Cs were suppressed in AtMYB20-OX and enhanced in AtMYB20-SRDX by NaCl treatment.•AtMYB20 binds to the ABI1 promoter region containing a MYB recognition element in vitro.•AtMYB20 binds to the ABI1 and AtPP2CA promoter regions containing an ACGT core element in vitro.•AtMYB20 acts as a negative regulator of PP2Cs to enhance salt tolerance. We have characterized the function of a plant R2R3-MYB transcription factor, Arabidopsis thaliana MYB20 (AtMYB20). Transgenic plants overexpressing AtMYB20 (AtMYB20-OX) enhanced salt stress tolerance while repression lines (AtMYB20-SRDX) were more vulnerable to NaCl than wild-type plants. Following NaCl treatment, the expressions of ABI1, ABI2 and AtPP2CA, which encode type 2C serine/threonine protein phosphatases (PP2Cs) that act as negative regulators in abscisic acid (ABA) signaling, were suppressed in AtMYB20-OX but induced in AtMYB20-SRDX. The electrophoretic mobility shift assay results revealed that AtMYB20 binds to the promoter regions containing the MYB recognition sequence (TAACTG) and an ACGT core element of ABI1 and AtPP2CA. These findings suggest that AtMYB20 down-regulates the expression of PP2Cs, the negative regulator of ABA signaling, and enhances salt tolerance.
ISSN:0014-5793
1873-3468
DOI:10.1016/j.febslet.2013.04.028