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Endogenous gibberellins affect root nodule symbiosis via transcriptional regulation of NODULE INCEPTION in Lotus japonicus
Author(s) -
Akamatsu Akira,
Nagae Miwa,
Nishimura Yuka,
Romero Montero Daniela,
Ninomiya Satsuki,
Kojima Mikiko,
Takebayashi Yumiko,
Sakakibara Hitoshi,
Kawaguchi Masayoshi,
Takeda Naoya
Publication year - 2021
Publication title -
the plant journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.058
H-Index - 269
eISSN - 1365-313X
pISSN - 0960-7412
DOI - 10.1111/tpj.15128
Subject(s) - biology , lotus japonicus , gibberellin , root nodule , microbiology and biotechnology , symbiosis , mutant , nodule (geology) , endogeny , rhizobia , rhizobium , gibberellic acid , transcription factor , botany , biochemistry , bacteria , gene , genetics , germination , paleontology
SUMMARY 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.