The intragenic suppressor mutation Leu59Phe compensates for the effect of detrimental mutations in the jasmonate receptor COI1

Abstract

The phytohormones jasmonates (JAs) control plant development, growth, and defense against insects and pathogens. The Arabidopsis JA receptor Coronatine Insensitive 1 (COI1) interacts with ARABIDOPSIS SKP-LIKE1 (ASK1)/ASK2 to form the SCF COI1 E3 ligase and mediate JA responses. Here, we performed a genetic suppressor screen using the leaky coi1-2 (COI1 Leu245Phe ) mutant for restored sensitivity to JA, and identified the intragenic suppressor mutation Leu59Phe, which was in the region connecting the F-box and leucinerich repeats domains of COI1. The L59F substitution not only restores the COI1 L245F function, but also the COI1 Gly434Glu (coi1-22 rsp ) function in JA responses, through recovering their interactions with ASK1 or ASK2 and their protein levels. The L59F change itself could not enhance the interactions between COI1 and ASK1/ 2, nor affect JA responses. The present study reveals that the Leu59Phe substitution compensates for the effect of some deleterious mutations in the JA receptor COI1.

Dual localization of JA receptor, CaCOI2, explains JA perception dynamics in chickpea

“…Considering CaCOI2 has a functional F-box and LRR region, the inactive behaviour of both chimeric proteins suggested that there can be multiple additional amino acid residues distributed along F-box and LRR region, which still needed to be identified as “critical” for their functionality as a JA receptor. These results were in agreement of previous reports where multiple alleles were found associated with the AtCOI1 activity (Feys et al, 1994; Yan et al, 2009; Sheard et al, 2010; Song et al, 2021). Hence, we mapped amino acid residues of CaCOI1 and CaCOI2 with previously identified atcoi1 alleles; however, none of these alleles explained the non-functional behaviour of CaCOI1 (Feys et al, 1994; Ellis and Turner, 2002; Yan et al, 2009; Acosta et al, 2013; Song et al, 2021, Figure S13).…”

“…These results were in agreement of previous reports where multiple alleles were found associated with the AtCOI1 activity (Feys et al, 1994; Yan et al, 2009; Sheard et al, 2010; Song et al, 2021). Hence, we mapped amino acid residues of CaCOI1 and CaCOI2 with previously identified atcoi1 alleles; however, none of these alleles explained the non-functional behaviour of CaCOI1 (Feys et al, 1994; Ellis and Turner, 2002; Yan et al, 2009; Acosta et al, 2013; Song et al, 2021, Figure S13). Interestingly, the CaCOI1 F-box -CaCOI2 LRR , though failed to interact with JAZ proteins, was able to localize to the nucleus on MeJA treatment, but CaCOI2 F-box -CaCOI1 LRR failed to penetrate the nuclear membrane (Figure 6B).…”

JAZ is essential for ligand specificity of the COI1/JAZ co-receptor

“…The crystal structure of A. thaliana COI1-JAZ complex showed that JA-Ile or its mimic COR bind the COI1 binding pocket and JAZ interacts with COI1 and the hormone, trapping the ligand in the COI1 pocket ( 7 ). Amino acid substitutions in the COI1 pocket result in changes in ligand specificity ( 8 , 26 ), whereas a mutation between the F-box and the Leucine-rich repeats (LRRs) restores the JA sensitivity of deleterious mutations in COI1 ( 27 ). From an evolutionary perspective, we previously demonstrated that a single amino acid change in COI1 was responsible for the switch in ligand specificity from dn-OPDA in bryophytes to JA-Ile in angiosperms ( 8 ).…”

A molecular framework for signaling crosstalk between jasmonate and ethylene in anthocyanin biosynthesis, trichome development, and defenses against insect herbivores in Arabidopsis

“…The Arabidopsis thaliana mutants coi1‐1 (Xie et al, 1998), coi1‐2 (Song et al, 2021), ein3‐1 (Chao et al, 1997), eil1‐3 /Salk_049679, ein3‐1 ein1‐3 (Song et al, 2014a), jaz1‐1/2‐2/5‐1/6‐5 , jaz10‐1/11‐1/12‐1 , jaz3‐5/4‐1/7‐1/9‐1 , jaz1‐1/2‐2/3‐5/4‐1/5‐1/6‐5/7‐1/9‐1/10‐1/11‐1/12‐1 , coi1‐1 jaz1‐1/2‐2/3‐5/4‐1/5‐1/6‐5/7‐1/9‐1/10‐1/11‐1/12‐1 (Liu et al, 2021), gl3 (WISCDSLOX412G05), egl3‐7 (Salk_077439), tt8 (Salk_082999), gl1 (Salk_039478), ttg1‐c1 , and transgenic plants overexpressing GL3 ( GL3OE ), EGL3 ( EGL3OE ), TT8 ( TT8OE ) (Qi et al, 2011), or 6 myc‐EGL3 under control of CaMV35S promoter were as previously described, obtained from Arabidopsis Biological Resource Center, generated by the clustered regularly interspaced palindromic repeats (CRISPR)/CRISPR‐associated protein 9 (Cas9) method (Wang et al, 2015; Yan et al, 2015) or by transformation of the constructs. Primers for vector construction are listed in Table S1.…”