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.