Plants are aerobic organisms that rely on molecular oxygen for respiratory energy production. Hypoxic conditions, with oxygen levels ranging between 1% and 5%, usually limit aerobic respiration and affect plant growth and development. Here, we demonstrate that the hypoxic microenvironment induced by active cell proliferation during the two-step plant regeneration process intrinsically represses the regeneration competence of the callus in . We showed that hypoxia-repressed plant regeneration is mediated by the RELATED TO APETALA 2.12 (RAP2.12) protein, a member of the Ethylene Response Factor VII (ERF-VII) family. We found that the hypoxia-activated RAP2.12 protein promotes salicylic acid (SA) biosynthesis and defense responses, thereby inhibiting pluripotency acquisition and shoot regeneration in calli. Molecular and genetic analyses revealed that RAP2.12 could bind directly to the () gene promoter and activate SA biosynthesis, repressing plant regeneration possibly via a PLETHORA (PLT)-dependent pathway. Consistently, the mutant calli exhibits enhanced shoot regeneration, which is impaired by SA treatment. Taken together, these findings uncover that the cell proliferation-dependent hypoxic microenvironment reduces cellular pluripotency and plant regeneration through the RAP2.12–SID2 module.

中文翻译：

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愈伤组织增殖诱导的缺氧微环境降低拟南芥芽再生能力

植物是需氧生物，依靠分子氧产生呼吸能。缺氧条件（氧气含量在 1% 到 5% 之间）通常会限制有氧呼吸并影响植物的生长和发育。在这里，我们证明，在两步植物再生过程中，活跃的细胞增殖诱导的缺氧微环境本质上抑制了愈伤组织的再生能力。我们发现缺氧抑制的植物再生是由与 APETALA 2.12 (RAP2.12) 相关的蛋白介导的，该蛋白是乙烯反应因子 VII (ERF-VII) 家族的成员。我们发现缺氧激活的 RAP2.12 蛋白促进水杨酸（SA）生物合成和防御反应，从而抑制愈伤组织中多能性的获得和芽再生。分子和遗传分析表明，RAP2.12 可以直接与 () 基因启动子结合并激活 SA 生物合成，可能通过 PLETHORA (PLT) 依赖性途径抑制植物再生。一致地，突变愈伤组织表现出增强的芽再生，而 SA 处理会损害这种再生。总而言之，这些发现揭示了细胞增殖依赖性缺氧微环境通过 RAP2.12-SID2 模块降低了细胞多能性和植物再生。