Endogenous salicylic acid suppresses de novo root regeneration from leaf explants

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Tran, Sorrel ; Ison, Madalene ; Dias, Nathalia Cassia Ferreira ; Ortega, Maria Andrea ; Chen, Yun-Fan Stephanie ; Peper, Alan ; Hu, Lanxi ; Xu, Dawei ; Mozaffari, Khadijeh ; Severns, Paul M. ; Yao, Yao ; Tsai, Chung-Jui ; Teixeira, Paulo Jose Pereira Lima ; Yang, Li

• Tipo de documento: Artigo Científico
• Fonte: PLOS GENETICS; v. 19, n. 3, p. 18-pg., 2023-03-01.

Resumo

Author summaryTissue regeneration is a core technology for modern agriculture and horticulture. It is widely used for crop improvement, propagation of valuable varieties and generation of chimeric plants. Plants must integrate physiological and environmental cues to complete this dramatic and sophisticated reprogramming process. Difficulties in regenerating adventitious roots from cuttings, such as the age-dependent decline of rooting, is still a bottleneck in propagating economically and ecologically important plants. We discovered that Salicylic acid (SA), a key hormone for plant defense, suppresses root regeneration from cuttings. Depleting endogenous SA or disrupting SA signaling enhances plants' regeneration ability. Our study provides new knowledge for overcoming challenges in vegetative propagation by manipulating the SA response. Plants can regenerate new organs from damaged or detached tissues. In the process of de novo root regeneration (DNRR), adventitious roots are frequently formed from the wound site on a detached leaf. Salicylic acid (SA) is a key phytohormone regulating plant defenses and stress responses. The role of SA and its acting mechanisms during de novo organogenesis is still unclear. Here, we found that endogenous SA inhibited the adventitious root formation after cutting. Free SA rapidly accumulated at the wound site, which was accompanied by an activation of SA response. SA receptors NPR3 and NPR4, but not NPR1, were required for DNRR. Wounding-elevated SA compromised the expression of AUX1, and subsequent transport of auxin to the wound site. A mutation in AUX1 abolished the enhanced DNRR in low SA mutants. Our work elucidates a role of SA in regulating DNRR and suggests a potential link between biotic stress and tissue regeneration. (AU)

• Processo FAPESP: 18/24432-0 - Estudo funcional de efetores de patógenos do cacaueiro e busca por receptores imunes mediadores de resistência
• Beneficiário: Paulo José Pereira Lima Teixeira
• Modalidade de apoio: Auxílio à Pesquisa - Jovens Pesquisadores