BREVIPEDICELLUS and ERECTA control the expression of AtPRX17 to prevent Arabidopsis callus browning
BREVIPEDICELLUS and ERECTA control the expression of AtPRX17 to prevent Arabidopsis callus browning
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BREVIPEDICELLUS 和 ERECTA 控制 AtPRX17 的表达以防止拟南芥愈伤组织褐变
DOI：
10.1093/jxb/erab512
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发表时间：
2022-01-15
影响因子：
6.9
通讯作者：
Zheng，Huiqiong
中科院分区：
文献类型：
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作者：
Xie，Junyan;Qi，Bin;Zheng，Huiqiong
有效的体外愈伤组织产生是组织培养繁殖所必需的，这是一个允许植物再生和转基因育种以获得所需表型的过程。鉴定防止愈伤组织生长受损和愈伤组织布朗宁的基因和调控元件对于体外愈伤组织系统的发展是必不可少的。在这里，我们表明，在拟南芥愈伤组织的BREVIPEDICELLUS和ERECTA途径收敛，以防止愈伤组织布朗宁，并积极调节过氧化物酶基因AtPRX 17在快速生长的愈伤组织的表达。短梗霉和毛梗霉的功能缺失突变导致愈伤组织布朗宁显著增加。在bp-5 er 105双突变体背景下表达35 S pro：：AtPRX 17的转基因株系完全挽救了这种表型异常。利用体内（染色质免疫沉淀-PCR和瞬时表达）和体外（电泳迁移率变动分析）测定，我们观察到短杆菌蛋白直接结合AtPRX 17的上游序列，促进其在愈伤组织生长过程中的转录。ERECTA是细胞增殖和生长所需的普遍存在的因子。我们发现ERECTA积极调节转录因子WRKY 6的表达，WRKY 6直接结合到AtPRX 17启动子上的一个单独位点，进一步增加其表达。我们的数据揭示了一个重要的分子机制参与调节过氧化物酶同工酶的表达，以减少拟南芥愈伤组织布朗宁。
Efficientin vitrocallus generation is required for tissue culture propagation, a process that allows for plant regeneration and transgenic breeding for desired phenotypes. Identifying genes and regulatory elements that prevent impaired callus growth and callus browning is essential for the development ofin vitrocallus systems. Here, we show that theBREVIPEDICELLUSandERECTApathways in Arabidopsis calli converge to prevent callus browning, and positively regulate the expression of the isoperoxidase geneAtPRX17in rapidly growing calli. Loss-of-function mutations in bothBREVIPEDICELLUSandERECTAresulted in markedly increased callus browning. Transgenic lines expressing35S pro::AtPRX17in thebp-5 er105double mutant background fully rescued this phenotypic abnormality. Usingin vivo(chromatin immunoprecipitation-PCR and transient expression) andin vitro(electrophoretic mobility shift assays) assays, we observed that the BREVIPEDICELLUS protein binds directly to the upstream sequence ofAtPRX17to promote its transcription during callus growth. ERECTA is a ubiquitous factor required for cell proliferation and growth. We show that ERECTA positively regulates the expression of the transcription factor WRKY6, which directly binds to a separate site on theAtPRX17promoter, further increasing its expression. Our data reveal an important molecular mechanism involved in the regulation of peroxidase isozyme expression to reduce Arabidopsis callus browning.