CEPs suppress auxin signaling but promote cytokinin signaling to inhibit root growth in Arabidopsis

• Published in: Biochemical and biophysical research communications 2024-06, Vol.711, p.149934, Article 149934
• Main Authors: Zhang, Yuwen, Duan, Xingliang, Wang, Zhen, Lv, Yuanda, Qi, Weicong, Li, Lun, Luo, Le, Xuan, Wei
• Format: Article
• Language: English
• Subjects: Arabidopsis (Arabidopsis thaliana); Auxin; CEP; Cytokinin; Root development
• ISSN: 0006-291X; 1090-2104; 1090-2104
• DOI: 10.1016/j.bbrc.2024.149934

C-terminally encoded peptides (CEPs) are peptide hormones that function as mobile signals coordinating crucial developmental programs in plants. Previous studies have revealed that CEPs exert negative regulation on root development through interaction with CEP receptors (CEPRs), CEP DOWNSTREAMs (CEPDs), the cytokinin receptor ARABIDOPSIS HISTIDINE KINASE (AHKs) and the transcriptional repressor Auxin/Indole-3-Acetic Acid (AUX/IAA). However, the precise molecular mechanisms underlying CEPs-mediated regulation of root development via auxin and cytokinin signaling pathways still necessitate further detailed investigation. In this study, we examined prior research and elucidated the underlying molecular mechanisms. The results showed that both synthetic AtCEPs and overexpression of AtCEP5 markedly supressed primary root elongation and lateral root (LR) formation in Arabidopsis. Molecular biology and genetics elucidated how CEPs inhibit root growth by suppressing auxin signaling while promoting cytokinin signaling. In summary, this study elucidated the inhibitory effects of AtCEPs on Arabidopsis root growth and provided insights into their potential molecular mechanisms, thus enhancing our comprehension of CEP-mediated regulation of plant growth and development. •Both synthetic AtCEPs and AtCEP5 overexpression suppress primary root elongation and lateral root formation.•The regulation of CEPs on root development requires their receptors CEPRs.•Molecular evidence reveals that CEPs inhibit root development by modulating auxin and cytokinin signaling.