Identification of JAZ-interacting MYC transcription factors involved in latex drainage in Hevea brasiliensis

Hevea brasiliensis Müll. Arg. is one of the most frequently wounded plants worldwide. Expelling latex upon mechanical injury is a wound response of rubber trees. However, JA-mediated wound responses in rubber trees are not well documented. In this work, three JAZ-interacting MYC transcription factor...

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Published inScientific reports Vol. 8; no. 1; pp. 909 - 13
Main Authors Zhai, Jinling, Hao, Hui, Xiao, Hua, Cao, Yuxin, Lin, Xiangui, Huang, Xi
Format Journal Article
LanguageEnglish
Published England Nature Publishing Group 17.01.2018
Nature Publishing Group UK
Nature Portfolio
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Summary:Hevea brasiliensis Müll. Arg. is one of the most frequently wounded plants worldwide. Expelling latex upon mechanical injury is a wound response of rubber trees. However, JA-mediated wound responses in rubber trees are not well documented. In this work, three JAZ-interacting MYC transcription factors of H. brasiliensis (termed HbMYC2/3/4) were identified by yeast two-hybrid screening. HbMYC2/3/4 each showed specific interaction profiles with HbJAZs. HbMYC2/3/4 each localized in the nucleus and exhibited strong transcriptional activity. To identify the target genes potentially regulated by HbMYC2/3/4, cis-elements interacting with HbMYC2/3/4 were first screened by yeast one-hybrid assays; the results indicated that HbMYC2/3/4 each could bind G-box elements. Additional analysis confirmed that HbMYC2/3/4 bound the HbPIP2;1 promoter, which contains five G-box cis-elements, and regulated the expression of reporter genes in yeast cells and in planta. HbMYC2/3/4 were induced by exogenous JA treatment but suppressed by ethylene (ET) treatment; in contrast, HbPIP2;1 was positively regulated by ET but negatively regulated by JA treatment. Given that HbPIP2;1 is involved in latex drainage, it could be proposed that HbMYC2/3/4 are involved in the regulation of HbPIP2;1 expression as well as latex drainage, both of which are coordinated by the JA and ET signalling pathways.
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ISSN:2045-2322
2045-2322
DOI:10.1038/s41598-018-19206-3