Auxin plays a critical role in lateral root (LR) formation. The signaling module composed of auxin-response factors (ARFs) and lateral organ boundaries domain transcription factors mediates auxin signaling to control almost every stage of LR 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 ERF13 results in restricted passage of the LR primordia through the endodermal layer, greatly reducing LR emergence, whereas the erf13 mutants showed an increase in emerged LR. ERF13 inhibits the expression of 3-ketoacyl-CoA synthase16 (KCS16), which encodes a fatty acid elongase involved in very-long-chain fatty acid (VLCFA) biosynthesis. Overexpression of KCS16 or exogenous VLCFA treatment rescues the LR emergence defects in ERF13 overexpression lines, indicating a role downstream of the auxin–MPK14–ERF13 signaling module. Collectively, our study uncovers a novel molecular mechanism by which MPK14-mediated auxin signaling modulates LR development via ERF13-regulated VLCFA biosynthesis.

生长素在侧根（LR）的形成中起关键作用。由生长素反应因子（ARF）和侧器官边界域转录因子组成的信号传导模块介导生长素信号传导，以控制LR发育的几乎每个阶段。在这里，我们显示生长素诱导的APETALA2 /乙烯反应因子（AP2 / ERF）转录因子ERF13的降解，取决于MITOGEN-活化的蛋白激酶MPK14介导的磷酸化，在LR发育中起重要作用。ERF13的过度表达导致LR原基通过内胚层的通过受到限制，大大减少了LR的出现，而erf13突变体则显示了LR的增加。ERF13抑制3-酮基-CoA合酶16（KCS16），其编码参与超长链脂肪酸（VLCFA）生物合成的脂肪酸延伸酶。KCS16的过表达或外源性VLCFA处理可挽救ERF13过表达株系中的LR出现缺陷，这表明生长素–MPK14–ERF13信号传导模块的下游发挥了作用。总的来说，我们的研究揭示了一种新的分子机制，通过该机制，MPK14介导的生长素信号传导通过ERF13调控的VLCFA生物合成来调节LR的发育。