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Rice ERECT LEAF 1 acts in an alternative brassinosteroid signaling pathway independent of the receptor kinase OsBRI1.

ABSTRACT: ERECT LEAF 1 (ELF1) was previously identified as a component of brassinosteroid signaling in rice. A double mutant obtained by crossing elf1-1 (a null mutant of ELF1) with d61-1 (a leaky mutant of OsBRI1) showed a more severe phenotype than did the elf1-1 single mutant, resembling that of a severe brassinosteroid-deficient mutant. Microarray analysis showed that the gene expression profile of elf1-1 was distinct from that of d61-12 (a leaky mutant of OsBRI1 with a phenotype similar to that of elf1-1), and fewer than half of genes differentially expressed between the wild-type and elf1-1 showed similar differences in d61-12 relative to the wild-type. These results indicate that less than half of ELF1-regulated genes in rice seedlings are affected by OsBRI1, and suggest that ELF1 acts in a rice brassinosteroid signaling pathway different from that initiated by OsBRI1. Gene expression analysis showed that some stress response-related genes were induced in elf1-1 but not in d61-12, and 8 of 9 genes oppositely regulated in elf1-1 and d61-12 were significantly up- or down-regulated in both elf1-1 and jasmonic acid-treated wild-type. These results imply that ELF1 suppresses stress-induced signalling, and that jasmonic acid signaling is stimulated in elf1-1; therefore, ELF1 may be involved in the brassinosteroid-mediated suppression of jasmonic acid response in rice.

SUBMITTER: Sakamoto T

PROVIDER: S-EPMC5792126 | biostudies-literature | 2017 Dec

REPOSITORIES: biostudies-literature

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Rice ERECT LEAF 1 acts in an alternative brassinosteroid signaling pathway independent of the receptor kinase OsBRI1.

Sakamoto Tomoaki T Kitano Hidemi H Fujioka Shozo S

Plant signaling & behavior 20171127 12

ERECT LEAF 1 (ELF1) was previously identified as a component of brassinosteroid signaling in rice. A double mutant obtained by crossing elf1-1 (a null mutant of ELF1) with d61-1 (a leaky mutant of OsBRI1) showed a more severe phenotype than did the elf1-1 single mutant, resembling that of a severe brassinosteroid-deficient mutant. Microarray analysis showed that the gene expression profile of elf1-1 was distinct from that of d61-12 (a leaky mutant of OsBRI1 with a phenotype similar to that of el ...[more]

PMID: 29172939

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Project description:Across metazoans, innate immunity is vital in defending organisms against viral infection. In mammals, antiviral innate immunity is orchestrated by interferon signaling, activating the STAT transcription factors downstream of the JAK kinases to induce expression of antiviral effector genes. In the nematode Caenorhabditis elegans, which lacks the interferon system, the major antiviral response so far described is RNA interference (RNAi), but whether additional gene expression responses are employed is not known. Here we show that, despite the absence of both interferon and JAK, the C. elegans STAT homolog STA-1 orchestrates antiviral immunity. Intriguingly, mutants lacking STA-1 are less permissive to antiviral infection. Using gene expression analysis and chromatin immunoprecipitation, we show that, in contrast to the mammalian pathway, STA-1 acts mostly as a transcriptional repressor. Thus, STA-1 might act to suppress a constitutive antiviral response in the absence of infection. Additionally, using a reverse genetic screen, we identify the kinase SID-3 as a new component of the response to infection, which, along with STA-1, participates in the transcriptional regulatory network of the immune response. Our work uncovers novel physiological roles for two factors in viral infection: a SID protein acting independently of RNAi and a STAT protein acting in C. elegans antiviral immunity. Together, these results illustrate the complex evolutionary trajectory displayed by innate immune signaling pathways across metazoan organisms.IMPORTANCE Since innate immunity was discovered, a diversity of pathways has arisen as powerful first-line defense mechanisms to fight viral infection. RNA interference, reported mostly in invertebrates and plants, as well as the mammalian interferon response and JAK/STAT pathway are key in RNA virus innate immunity. We studied infection by the Orsay virus in Caenorhabditis elegans, where RNAi is known to be a potent antiviral defense. We show that, in addition to its RNAi pathway, C. elegans utilizes an alternative STAT pathway to control the levels of viral infection. We identify the transcription factor STA-1 and the kinase SID-3 as two components of this response. Our study defines C. elegans as a new example of the diversity of antiviral strategies.

Dataset Information

Rice ERECT LEAF 1 acts in an alternative brassinosteroid signaling pathway independent of the receptor kinase OsBRI1.

Publications

Rice ERECT LEAF 1 acts in an alternative brassinosteroid signaling pathway independent of the receptor kinase OsBRI1.

Similar Datasets

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