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Acquired thermotolerance independent of heat shock factor A1 (HsfA1), the master regulator of the heat stress response.

ABSTRACT: The heat stress (HS) response in eukaryotes is mainly regulated by heat shock factors (HSFs). Genetic disruption of the master HSF gene leads to dramatically reduced HS response and thermotolerance in several model organisms. However, it is not clear whether organisms devoid of the master regulator can still acclimate to heat. Previously, we showed that Arabidopsis HsfA1a, HsfA1b, and HsfA1d act as master regulators in the HS response. In this study, we examined the heat acclimation capacity of the Arabidopsis quadruple and triple T-DNA knockout mutants of HsfA1a, HsfA1b, HsfA1d, and HsfA1e. Our data showed that in the absence of the master regulators, a minimal but significant level of acquired thermotolerance could be attained in the Arabidopsis mutants after acclimation. The optimum acclimation temperature for the HsfA1 quadruple mutant was lower than that for the wild type plants, suggesting that plant cells have two HS-sensing mechanisms that can be distinguished genetically. The acquired thermotolerance of the quadruple mutant was likely due to the induction of a small number of HsfA1-independent HS response genes regulated by other transcription factors. Here, we discuss the possible candidates and propose a working model of the transcription network of the HS response by including the HsfA1-dependent and -independent pathways.

SUBMITTER: Liu HC

PROVIDER: S-EPMC3419016 | biostudies-literature | 2012 May

REPOSITORIES: biostudies-literature

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Acquired thermotolerance independent of heat shock factor A1 (HsfA1), the master regulator of the heat stress response.

Liu Hsiang-chin HC Charng Yee-yung YY

Plant signaling & behavior 20120420 5

The heat stress (HS) response in eukaryotes is mainly regulated by heat shock factors (HSFs). Genetic disruption of the master HSF gene leads to dramatically reduced HS response and thermotolerance in several model organisms. However, it is not clear whether organisms devoid of the master regulator can still acclimate to heat. Previously, we showed that Arabidopsis HsfA1a, HsfA1b, and HsfA1d act as master regulators in the HS response. In this study, we examined the heat acclimation capacity of ...[more]

PMID: 22516818

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Project description:A hallmark feature of Mycobacterium tuberculosis pathogenesis lies in the ability of the pathogen to survive within macrophages under a stressful environment. Thus, coordinated regulation of stress proteins is critically important for an effective adaptive response of M. tuberculosis, the failure of which results in elevated immune recognition of the tubercle bacilli with reduced survival during chronic infections. Here, we show that virulence regulator PhoP impacts the global regulation of heat shock proteins, which protect M. tuberculosis against stress generated by macrophages during infection. Our results identify that in addition to classical DNA-protein interactions, newly discovered protein-protein interactions control complex mechanisms of expression of heat shock proteins, an essential pathogenic determinant of M. tuberculosis While the C-terminal domain of PhoP binds to its target promoters, the N-terminal domain of the regulator interacts with the C-terminal end of the heat shock repressors. Remarkably, our findings delineate a regulatory pathway which involves three major transcription factors, PhoP, HspR, and HrcA, that control in vivo recruitment of the regulators within the target genes and regulate stress-specific expression of heat shock proteins via protein-protein interactions. The results have implications on the mechanism of regulation of PhoP-dependent stress response in M. tuberculosisIMPORTANCE The regulation of heat shock proteins which protect M. tuberculosis against stress generated by macrophages during infection is poorly understood. In this study, we show that PhoP, a virulence regulator of the tubercle bacilli, controls heat shock-responsive genes, an essential pathogenic determinant of M. tuberculosis Our results unravel that in addition to classical DNA-protein interactions, complex mechanisms of regulation of heat shock-responsive genes occur through multiple protein-protein interactions. Together, these findings delineate a fundamental regulatory pathway where transcription factors PhoP, HspR, and HrcA interact with each other to control stress-specific expression of heat shock proteins.

Project description:BACKGROUND:Agriculture is highly dependent on climate. Increases in temperature caused by global warming pose challenges for crop production. Heat stress induces oxidative damage to cell membranes and then causes cell death. Plants have developed various responses to elevated temperatures, including hormone signaling pathways and heat shock factors that elevate their thermotolerance. In response to heat stress, the gaseous hormone ethylene is produced through regulation of the expression of signaling-related genes to modulate resource allocation dynamics. For comprehensive understanding of the role of ethylene, this study used an ethylene precursor to analyze the ethylene signaling pathway involved in adjustment of the homeostasis of the antioxidant system and to evaluate heat shock factor expression in rice seedlings under heat stress. RESULTS:Levels of cell membrane oxidation and ion leakage were reduced in rice seedlings under heat treatment combined with ethylene precursor treatment, conferring enhanced thermotolerance. Reduction of the fresh weight and chlorophyll a/b ratio in rice seedlings was lower in rice seedlings under heat stress with ethylene precursor treatment than in those under heat stress only. Moreover, reduction of antioxidant response caused by heat stress was ameliorated by treatment with ethylene precursors such as catalase and total peroxidase. Quantitative reverse transcriptase-polymerase chain reaction showed higher expression levels of heat shock factors such as HSFA1a and HSFA2a, c, d, e, and f and ethylene-signaling-related genes such as ethylene insensitive 2, ethylene insensitive-like 1, and ethylene insensitive-like 2 in rice seedlings under heat stress with ethylene precursor treatment than in rice seedlings under heat stress only. CONCLUSION:Ethylene-mediated signaling was involved in the reduction of oxidative damage, maintenance of chlorophyll content, and enhancement of thermotolerance in rice seedlings under heat stress. Furthermore, this study revealed heat shock factors and ethylene-signaling-related genes involved in complex network regulation that confers thermotolerance to rice seedlings.

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Acquired thermotolerance independent of heat shock factor A1 (HsfA1), the master regulator of the heat stress response.

Publications

Acquired thermotolerance independent of heat shock factor A1 (HsfA1), the master regulator of the heat stress response.

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