The TaCEP15 peptide signaling cascade modulates primary root length and drought tolerance in wheat.

Abstract

Drought stress poses an environmental challenge affecting crop yield. Small signaling peptides play crucial roles in the regulation of stress responses in plants. Here, we unveil that the TaCEP15 peptide interacts with the leucine-rich repeat receptor-like kinase TaCEPRL. Knockout of <i>TaCEP15</i> or <i>TaCEPRL</i> increases primary root length and enhances drought tolerance in wheat. TaCEPRL interacts with and phosphorylates TaSnRK1α, leading to the degradation of TaSnRK1α. The presence of TaCEP15 intensifies the phosphorylation and degradation of TaSnRK1α. Consistently, overexpressing <i>TaSnRK1</i>α boosts primary root elongation and augments drought tolerance. In addition, we identify the transcription factor TabZIP9, which binds to the <i>TaCEP15</i> promoter and suppresses its transcription. A-to-T substitution in the <i>TaCEP15</i> promoter decreases the binding affinity of TabZIP9. As expected, transgenic plants with <i>TabZIP9</i> knockout or overexpression exhibit noteworthy changes in primary root length and drought tolerance. Our findings shed light on the importance of the peptide signaling pathway in regulating primary root length and responding to drought stress in wheat.