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Information Journal Paper

Title

The evaluation of jasmonate signaling in Arabidopsis of a wild-type and mutants under salt, drought, IAA, ABA, and Pseudomonas aeruginosa stress

Pages

  115-134

Abstract

 Objective
Coronatine insensitive 1 (COI1) gene, insensitive to bacterial toxin, the main member of jasmonates (JAs), is closely related to biotic and abiotic resistance of plants. COI1 gene acts as the main controller of plant responses regulated by JA. To better understand the molecular basis of JA function, mutant and wild type in Arabidopsis were investigated under biotic and abiotic stresses.
Materials and methods
In this research, coi1 gene mutation and wild type were evaluated under Pseudomonas aeruginosa, IAA, ABA, salinity and drought stresses. Also, the physiological traits of mutant and wild type were investigated under the mentioned stress. In addition, the expression profile of JA-related genes in Arabidopsis leaves under five stresses was analyzed.
Results
The expression level of five genes in the leaves decreased in the mutant and increased in the wild type. The transcript levels of five genes related to (JA fatty acid desaturase, defective anther opening 1, allene oxide synthase, PDA reductase and 13-lipoxygenase) were well correlated with JA accumulation under five stresses. Compared to the wild type, the activities of catalase (CAT), peroxidase (PRO) and ascorbate peroxidase (APX) were high in coi1 mutant leaves under five stresses. Under these stresses, Arabidopsis plants produce much higher levels of Anthocyanins in the wild type compared to the coi1 mutant. The expression of other Anthocyanin biosynthetic genes was also induced by JA and dependent on COI1. These results showed that jasmonates may regulate the growth of Arabidopsis. For the first time in this study, the effect of Pseudomonas aeruginosa in coi1 mutant and wild type has been compared. The findings of the present study showed that Pseudomonas aeruginosa had the effect of cronotine by strengthening a COI-dependent pathway for pathogen proliferation, and the wild type had a high gene expression of jasmonic acid compared to the mutant. These results confirmed that the COI pathway was caused the proliferation of pathogens and the mutant type is more resistant to Pseudomonas aeruginosa than the wild type.
Conclusions
The results of the present study provide new insight into JA accumulation and its potential roles during development. These results indicated that jasmonate biosynthesis and signaling could be regulated by a complex regulatory network

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