Callus proliferation-induced hypoxic microenvironment decreases shoot regeneration competence in Arabidopsis
作者机构:Department of ChemistrySeoul National UniversitySeoul 08826Korea Plant Genomics and Breeding InstituteSeoul National UniversitySeoul 08826Korea Research Institute of Basic SciencesSeoul National UniversitySeoul 08826Korea
出 版 物:《Molecular Plant》 (分子植物(英文版))
年 卷 期:2024年第17卷第3期
页 面:395-408页
核心收录:
学科分类:0710[理学-生物学] 071001[理学-植物学] 07[理学]
基 金:funded by the Samsung Science and Technology Foundation(South Korea)under Project Number SSTF-BA2001-10 by the New Breeding Technologies Development Program(RS-2024-00322275)of the Rural Development Administration,South Korea
主 题:callus cell proliferation-induced hypoxia SID2 plant regeneration salicylic acid RAP2.12
摘 要:Plants are aerobic organisms that rely on molecular oxygen for respiratory energy *** conditions,with oxygen levels ranging between 1%and 5%,usually limit aerobic respiration and affect plant growth and ***,we demonstrate that the hypoxic microenvironment induced by active cell proliferation during the two-step plant regeneration process intrinsically represses the regener-ation competence of the callus in Arabidopsis *** showed that hypoxia-repressed plant regener-ation is mediated by the RELATED TO APETALA2.12(RAP2.12)protein,a memberof the Ethylene Response Factor VIl(ERF-Vll)*** found that the hypoxia-activated RAP2.12 protein promotes salicylic acid(SA)biosynthesis and defense responses,thereby inhibiting pluripotency acquisition and de novo shoot regeneration in *** and genetic analyses revealed that RAP2.12 could bind directly to the SALICYLIC ACID INDUCTION DEFICIENT 2(SID2)gene promoter and activate SA biosynthesis,repressing plant regeneration possibly via a PLETHORA(PLT)-dependent ***,the rap2.12 mutant calli exhibits enhanced shoot regeneration,which is impaired by SA *** together,these find-ings uncover that the cell proliferation-dependent hypoxic microenvironment reduces cellular pluripotency and plant regeneration through the RAP2.12-SID2 module.