生长素在侧根形成中起关键作用。由生长素反应因子(ARFs)-侧器官边界-结构域转录因子(LBDs)组成的信号模块介导生长素信号来控制IR发育的几乎每个阶段。本研究，我们研究表明生长素诱导的APETALA22/乙烯反应因子AP2/ER R转录因子ERF13的降解，这个过程依赖于丝裂原活化蛋白激酶MPK14的磷酸化介导，表明ERF13在LR发育中起着重要作用。ERF13的过表达导致LR原基(LRP)通过内胚层的通道受到限制，导致LR的出现大大减少。ERF13抑制3-酮酰基CoA合酶6(KCSi6)的表达，而KCS16编码一种参与超长链脂肪酸（VLCFAs）生物合成的脂肪酸延伸酶。
KCS16过表达或外源VLCFAs处理能互补ERF13过表达系中的LR缺陷表型，表明KCS16位于生长素-MPK14-ERF13在下游作用。总之，本研究揭示了MPK14介导的生长素信号通过ERF13调节的VLCFAs生物合成在LR发育中的新的分子机制。
Auxin plays a critical role in lateral root(LR)formation.The signaling module composed of auxin responsive factors(ARFs)-lateral organ boundaries-domain transcription factors(LBDs) mediates auxin signaling to control almost every stage of IR development.Here,we show that auxin-induced degradation of the APETALA2/Ethylene Responsive Factor(AP2/ERF) transcription factor ERF13, dependent on MITOGEN-ACTIVATED PROTEIN KINASE MPK14-mediated phosphorylation,plays an essential role in LR development.Overexpression of ERFrg results in restricted passage of the LR primordia(LRP)through the endodermal layer,leading to highly reduced LR emergence.ERF13 inhibits the expression of 3-ketoacyl-CoA synthaser6(KCSi6), which encodes a fatty acid elongase involved in very-long-chain fatty acids(VLCFAs)biosynthesis.
Overexpression of KCS16 or exogenous VILCFAs treatment rescues the LR emergence defects in ERFi3 overexpression lines,indicating a role downstream of the auxin-MPK14-ERF13 signaling module.In conclusion,this study uncovers a novel molecular mechanism of MPK14-mediated auxin signaling in LR development via ERF13-regulated VLCFAs biosynthesis.
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