Abstract
The identification of heat stress (HS)-resilient germplasm is important to ensure food security under less favorable environmental conditions. For that, germplasm with an altered activity of factors regulating the HS response is an important genetic tool for crop improvement. Heat shock binding protein (HSBP) is one of the main negative regulators of HS response, acting as a repressor of the activity of HS transcription factors. We identified a TILLING allele of Solanum lycopersicum (tomato) HSBP1. We examined the effects of the mutation on the functionality of the protein in tomato protoplasts, and compared the thermotolerance capacity of lines carrying the wild-type and mutant alleles of HSBP1. The methionine-to-isoleucine mutation in the central heptad repeats of HSBP1 leads to a partial loss of protein function, thereby reducing the inhibitory effect on Hsf activity. Mutant seedlings show enhanced basal thermotolerance, while mature plants exhibit increased resilience in repeated HS treatments, as shown by several physiological parameters. Importantly, plants that are homozygous for the wild-type or mutant HSBP1 alleles showed no significant differences under non-stressed conditions. Altogether, these results indicate that the identified mutant HSBP1 allele can be used as a genetic tool in breeding, aiming to improve the thermotolerance of tomato varieties.
Highlights
Heat stress (HS) is one of the most devastating environmental stresses that a plant can face during its life cycle
We explored the capacity of ethyl methanesulfonate (EMS)-induced mutations in the Heat shock binding protein (HSBP) coding gene to have a positive impact on the thermotolerance of tomato plants
As HSBPs are considered negative regulators of HS transcription factor (Hsf) and of the transcription of heat stress (HS)-induced genes, we examined the correlation of SlHSBP1 with that of all tomato
Summary
Heat stress (HS) is one of the most devastating environmental stresses that a plant can face during its life cycle. HS impacts membrane fluidity, microtubule organization and activity, and the general stability of enzymes participating in a variety of physiological processes [1,2,3]. High temperatures negatively affect the growth of vegetative and floral organs, induce flower abortion, and cause deviations from physiological developmental transitions, including gametophytic defects [4,5,6,7]. HS causes the accumulation of misfolded proteins, which is a condition referred to as proteotoxicity. This hampers the functionality and stability of structural, enzymatic, and regulatory proteins [8]. Protection and recovery from HS depend on the activation of a complex
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