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Endogenous gibberellins affect root nodule symbiosis via transcriptional regulation of NODULE INCEPTION in Lotus japonicus
The Plant Journal ( IF 6.2 ) Pub Date : 2020-12-10 , DOI: 10.1111/tpj.15128
Akira Akamatsu 1 , Miwa Nagae 2 , Yuka Nishimura 1 , Daniela Romero Montero 1 , Satsuki Ninomiya 1 , Mikiko Kojima 3 , Yumiko Takebayashi 3 , Hitoshi Sakakibara 3, 4 , Masayoshi Kawaguchi 2 , Naoya Takeda 1
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Legumes and nitrogen‐fixing rhizobial bacteria establish root nodule symbiosis, which is orchestrated by several plant hormones. Exogenous addition of biologically active gibberellic acid (GA) is known to inhibit root nodule symbiosis. However, the precise role of GA has not been elucidated because of the trace amounts of these hormones in plants and the multiple functions of GAs. Here, we found that GA signaling acts as a key regulator in a long‐distance negative‐feedback system of root nodule symbiosis called autoregulation of nodulation (AON). GA biosynthesis is activated during nodule formation in and around the nodule vascular bundles, and bioactive GAs accumulate in the nodule. In addition, GA signaling induces expression of the symbiotic transcription factor NODULE INCEPTION (NIN) via a cis‐acting region on the NIN promoter. Mutants with deletions of this cis‐acting region have increased susceptibility to rhizobial infection and reduced GA‐induced CLE‐RS1 and CLE‐RS2 expression, suggesting that the inhibitory effect of GAs occurs through AON. This is supported by the GA‐insensitive phenotypes of an AON‐defective mutant of HYPERNODULATION ABERRANT ROOT FORMATION1 (HAR1) and a reciprocal grafting experiment. Thus, endogenous GAs induce NIN expression via its GA‐responsive cis‐acting region, and subsequently the GA‐induced NIN activates the AON system to regulate nodule formation.

中文翻译:

内源性赤霉素通过对莲藕根瘤诱导的转录调控影响根瘤共生

豆科植物和固氮根瘤菌建立根瘤共生,这是由几种植物激素协调的。已知外源添加生物活性赤霉酸 (GA) 可抑制根瘤共生。然而,由于植物中这些激素的微量以及 GA 的多种功能,GA 的确切作用尚未阐明。在这里,我们发现 GA 信号在根结节共生的长距离负反馈系统中起着关键调节作用,称为结节自动调节(AON)。在结节维管束内和周围形成结节期间,GA生物合成被激活,并且生物活性GA在结节中积累。此外,GA 信号诱导共生转录因子NODULE INCEPTIONNIN) 通过NIN启动子上的顺式作用区域。具有该顺式作用区缺失的突变体对根瘤菌感染的易感性增加,并降低了 GA 诱导的CLE-RS1CLE-RS2表达,表明GA的抑制作用是通过 AON 发生的。这得到了 HYPERNODULATION ABERRANT ROOT FORMATION1 (HAR1) 的 AON 缺陷突变体的 GA 不敏感表型和相互移植实验的支持。因此,内源性GA 通过其 GA 响应顺式作用区诱导NIN表达,随后 GA 诱导的 NIN 激活 AON 系统以调节结节形成。
更新日期:2020-12-10
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