Endogenous gibberellins affect root nodule symbiosis via transcriptional regulation of NODULE INCEPTION in Lotus japonicus

Endogenous gibberellins affect root nodule symbiosis via transcriptional regulation of NODULE INCEPTION in Lotus japonicus
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内源赤霉素通过对荷花根瘤起始的转录调控影响根瘤共生

DOI:
10.1111/tpj.15128
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发表时间:
2021-01-09
期刊:
影响因子:
7.2
通讯作者:
Takeda, Naoya
Takeda, Naoya
中科院分区:
生物学1区
文献类型:
--
作者:
Akamatsu, Akira;Nagae, Miwa;Takeda, Naoya

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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。外源添加具有生物活性的赤霉酸(GA)可以抑制根瘤共生。然而,GA的确切作用尚未阐明,因为这些激素在植物中的痕量和GA的多种功能。在这里,我们发现,GA信号作为一个关键的调节器在一个长距离的负反馈系统的根瘤共生称为自动调节(AON)。在根瘤维管束内和周围的根瘤形成过程中,GA生物合成被激活,并且生物活性GA在根瘤中积累。此外,GA信号通过NIN启动子上的顺式作用区诱导共生转录因子NIN(NIN)的表达。该顺式作用区缺失的突变体增加了对根瘤菌感染的易感性,并降低了GA诱导的CLE-RS 1和CLE-RS 2表达,这表明GA的抑制作用是通过AON发生的。这一点得到了超节化畸形根形成1(HAR 1)AON缺陷突变体的GA不敏感表型和相互嫁接实验的支持。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。
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.