A missense mutation in CHS1, a TIR‐NB protein, induces chilling sensitivity in Arabidopsis

Abstract

SUMMARYLow temperature is an environmental factor that affects plant growth and development and plant-pathogen interactions. How temperature regulates plant defense responses is not well understood. In this study, we characterized chilling-sensitive mutant 1 (chs1), and functionally analyzed the role of the CHS1 gene in plant responses to chilling stress. The chs1 mutant displayed a chilling-sensitive phenotype, and also displayed defense-associated phenotypes, including extensive cell death, the accumulation of hydrogen peroxide and salicylic acid, and an increased expression of PR genes: these phenotypes indicated that the mutation in chs1 activates the defense responses under chilling stress. A map-based cloning analysis revealed that CHS1 encodes a TIR-NB-type protein. The chilling sensitivity of chs1 was fully rescued by pad4 and eds1, but not by ndr1. The overexpression of the TIR and NB domains can suppress the chs1-conferred phenotypes. Interestingly, the stability of the CHS1 protein was positively regulated by low temperatures independently of the 26S proteasome pathway. This study revealed the role of a TIR-NB-type gene in plant growth and cell death under chilling stress, and suggests that temperature modulates the stability of the TIR-NB protein in Arabidopsis.

ABA Regulation of the Cold Stress Response in Plants

“…For example, overexpression of antioxidant-defensive genes enhances chilling tolerance in maize and soybean (Van Breusegem et al 1999;Kocsy et al 2001), whereas repression of catalase gene expression reduces chilling tolerance (Kerdnaimongkol and Woodson 1999). Arabidopsis chs (chilling-sensitive) mutants display increased sensitivity to chilling temperature, which is at least partially due to the excessive accumulation of H 2 O 2 in chs mutant seedlings (Huang et al 2010a, b;Wang et al 2013;Yang et al 2010). Recent studies also show that ROS act as signal molecules mediating cold stress-signal transduction.…”

“…Cold stress induces the accumulation of SA in Arabidopsis, whereas SA-deficient mutants show increased growth in response to cold (Scott et al 2004). Gain of function of R/R-like protein mutants that overproduce SA, such aschs1, chs2, and chs3, display chillingsensitive phenotypes that are partially dependent upon SA (Huang et al 2010a;Yang et al 2010;Wang et al 2013). Indeed, there appears to be an optimal threshold of endogenous SA that is crucial for the chilling-dependent inhibition of plant growth.…”

Effector-Triggered Immunity: From Pathogen Perception to Robust Defense

“…Proteins analogous to mammalian signaling adaptors, which initiate downstream pathways by homotypic interactions with receptors, have not been identified in plants (90), although plant genomes contain truncated NLR genes that might naturally serve adaptor functions in resistance (55,64). Genetic and molecular analyses have shown that two truncated forms, the Arabidopsis cytoplasmic TIR-NB protein CHS1 (chilling sensitive 1) and the related TIR-NB CHL1 (CHS1-like 1), are important for restricting TNL immunity to maintain plant growth and fitness over a range of environmental conditions (144,156). Other truncated variants produced by TNL mRNA alternative splicing promote TNL resistance once ETI is initiated (36,74,158).…”

Mighty Dwarfs: Arabidopsis Autoimmune Mutants and Their Usages in Genetic Dissection of Plant Immunity

“…CHS1 encodes a truncated TIR-NB protein. A missense mutation in CHS1 results in activation of cell death and defense responses at low temperature (Wang et al, 2013; Zbierzak et al, 2013). …”