HY5 inhibits in vitro shoot stem cell niches initiation via directly repressing pluripotency and cytokinin pathways

HY5 inhibits in vitro shoot stem cell niches initiation via directly repressing pluripotency and cytokinin pathways
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DOI:
10.1111/tpj.15703
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发表时间:
2022-03-01
期刊:
影响因子:
7.2
通讯作者:
Xiang, Fengning
Xiang, Fengning
中科院分区:
生物学1区
文献类型:
--
作者:
Dai, Xuehuan;Wang, Jing;Xiang, Fengning

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外植体再生植物的效率受到植物激素和环境条件的影响。光对体外芽再生具有特别显着的影响,一些光信号因子参与芽再生,但潜在的分子机制仍然难以捉摸。在这里,ELONGATED HYPOCOTYL5 (HY5) 作为光信号传导的关键转录因子,被发现在一系列光照条件下抑制芽再生。 hy5-215突变体增强的芽再生能力在黑暗中不如在光下明显,表明HY5介导的芽再生抑制部分依赖于光。发现 WUSCHEL (WUS) 和 CLAVATA3 (CLV3) 表达的共定位与芽再生期间根外植体中干细胞生态位的启动一致。 HY5可以通过结合CLV3和WUS各自的启动子来直接抑制它们的表达。与此同时,HY5 通过与拟南芥响应调节器 12 (ARR12) 启动子结合,间接抑制 CLV3 和 WUS。 HY5 对 WUS 和 CLV3 产生的双重调节阻碍了芽干细胞生态位的启动。鉴定出一条 HY5 介导的抑制途径,该途径将细胞分裂素信号传导与芽再生过程中的多能性途径联系起来。
The efficiency of plant regeneration from explants is influenced by phytohormones and environmental conditions. Light has a particularly marked effect on in vitro shoot regeneration, and some light signaling factors are involved in shoot regeneration, while the underlying molecular mechanism remains elusive. Here, ELONGATED HYPOCOTYL5 (HY5), as the key transcription factor of light signaling, was found to inhibit shoot regeneration under a range of light conditions. The heightened shoot regeneration capacity of the hy5-215 mutant was less marked in the dark than in the light, showing that HY5-mediated inhibition of shoot regeneration is partly light dependent. The co-localization of WUSCHEL (WUS) and CLAVATA3 (CLV3) expressions was found to coincide with the initiation of stem cell niches in root explants during shoot regeneration. HY5 could directly repress CLV3 and WUS expression by binding to their respective promoters. In parallel, HY5 indirectly repressed CLV3 and WUS by binding to the ARABIDOPSIS RESPONSE REGULATOR12 (ARR12) promoter. The resulting dual regulation exerted by HY5 on WUS and CLV3 impeded the initiation of shoot stem cell niches. A HY5-mediated inhibitory pathway was identified that links cytokinin signaling and the pluripotency pathway during shoot regeneration.