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MYB30 transcription factor regulates oxidative and heat stress responses through ANNEXIN‐mediated cytosolic calcium signaling in Arabidopsis
Author(s) -
Liao Chancan,
Zheng Yuan,
Guo Yan
Publication year - 2017
Publication title -
new phytologist
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.742
H-Index - 244
eISSN - 1469-8137
pISSN - 0028-646X
DOI - 10.1111/nph.14679
Subject(s) - cytosol , microbiology and biotechnology , transcription factor , arabidopsis , calcium , calcium signaling , mutant , biology , signal transduction , biochemistry , chemistry , gene , enzyme , organic chemistry
Summary Cytosolic calcium signaling is critical for regulating downstream responses in plants encountering unfavorable environmental conditions. In a genetic screen for Arabidopsis thaliana mutants defective in stress‐induced cytosolic free Ca 2+ ([Ca 2+ ] cyt ) elevations, we identified the R2R3‐MYB transcription factor MYB30 as a regulator of [Ca 2+ ] cyt in response to H 2 O 2 and heat stresses. Plants lacking MYB30 protein exhibited greater elevation of [Ca 2+ ] cyt in response to oxidative and heat stimuli. Real‐time reverse transcription−polymerase chain reaction (RT‐PCR) results indicated that the expression of a number of ANNEXIN ( ANN ) genes, which encode Ca 2+ ‐regulated membrane‐binding proteins modulating cytosolic calcium signatures, were upregulated in myb30 mutants. Further analysis showed that MYB30 bound to the promoters of ANN1 and ANN4 and repressed their expression. myb30 mutants were sensitive to methyl viologen (MV) and heat stresses. The H 2 O 2 ‐ and heat‐induced abnormal [Ca 2+ ] cyt in myb30 was dependent on the function of ANN proteins. Moreover, the MV and heat sensitivity of myb30 was suppressed in mutants lacking ANN function or by application of LaCl 3 , a calcium channel blocker. These results indicate that MYB30 regulates oxidative and heat stress responses through calcium signaling, which is at least partially mediated by ANN1 and ANN4.