scholarly journals Regulation of Heat Shock Factor Pathways by γ-aminobutyric Acid (GABA) Associated with Thermotolerance of Creeping Bentgrass

2019 ◽  
Vol 20 (19) ◽  
pp. 4713 ◽  
Author(s):  
Ting Liu ◽  
Zhaoqiao Liu ◽  
Zhou Li ◽  
Yan Peng ◽  
Xinquan Zhang ◽  
...  

Activation and enhancement of heat shock factor (HSF) pathways are important adaptive responses to heat stress in plants. The γ-aminobutyric acid (GABA) plays an important role in regulating heat tolerance, but it is unclear whether GABA-induced thermotolerance is associated with activation of HSF pathways in plants. In this study, the changes of endogenous GABA level affecting physiological responses and genes involved in HSF pathways were investigated in creeping bentgrass during heat stress. The increase in endogenous GABA content induced by exogenous application of GABA effectively alleviated heat damage, as reflected by higher leaf relative water content, cell membrane stability, photosynthesis, and lower oxidative damage. Contrarily, the inhibition of GABA accumulation by the application of GABA biosynthesis inhibitor further aggravated heat damage. Transcriptional analyses showed that exogenous GABA could significantly upregulate transcript levels of genes encoding heat shock factor HSFs (HSFA-6a, HSFA-2c, and HSFB-2b), heat shock proteins (HSP17.8, HSP26.7, HSP70, and HSP90.1-b1), and ascorbate peroxidase 3 (APX3), whereas the inhibition of GABA biosynthesis depressed these genes expression under heat stress. Our results indicate GABA regulates thermotolerance associated with activation and enhancement of HSF pathways in creeping bentgrass.

Molecules ◽  
2021 ◽  
Vol 26 (17) ◽  
pp. 5337
Author(s):  
Cheng Huang ◽  
Yulong Tian ◽  
Bingbing Zhang ◽  
Muhammad Jawad Hassan ◽  
Zhou Li ◽  
...  

Chitosan (CTS) is a deacetylated derivative of chitin that is involved in adaptive response to abiotic stresses. However, the regulatory role of CTS in heat tolerance is still not fully understood in plants, especially in grass species. The aim of this study was to investigate whether the CTS could reduce heat-induced senescence and damage to creeping bentgrass associated with alterations in antioxidant defense, chlorophyll (Chl) metabolism, and the heat shock pathway. Plants were pretreated exogenously with or without CTS (0.1 g L−1) before being exposed to normal (23/18 °C) or high-temperature (38/33 °C) conditions for 15 days. Heat stress induced detrimental effects, including declines in leaf relative water content and photochemical efficiency, but significantly increased reactive oxygen species (ROS) accumulation, membrane lipid peroxidation, and Chl loss in leaves. The exogenous application of CTS significantly alleviated heat-induced damage in creeping bentgrass leaves by ameliorating water balance, ROS scavenging, the maintenance of Chl metabolism, and photosynthesis. Compared to untreated plants under heat stress, CTS-treated creeping bentgrass exhibited a significantly higher transcription level of genes involved in Chl biosynthesis (AsPBGD and AsCHLH), as well as a lower expression level of Chl degradation-related gene (AsPPH) and senescence-associated genes (AsSAG12, AsSAG39, Asl20, and Ash36), thus reducing leaf senescence and enhancing photosynthetic performance under heat stress. In addition, the foliar application of CTS significantly improved antioxidant enzyme activities (SOD, CAT, POD, and APX), thereby effectively reducing heat-induced oxidative damage. Furthermore, heat tolerance regulated by the CTS in creeping bentgrass was also associated with the heat shock pathway, since AsHSFA-6a and AsHSP82 were significantly up-regulated by the CTS during heat stress. The potential mechanisms of CTS-regulated thermotolerance associated with other metabolic pathways still need to be further studied in grass species.


2006 ◽  
Vol 290 (6) ◽  
pp. C1625-C1632 ◽  
Author(s):  
Angela L. Morrison ◽  
Martin Dinges ◽  
Kristen D. Singleton ◽  
Kelli Odoms ◽  
Hector R. Wong ◽  
...  

Glutamine (GLN) has been shown to protect cells, tissues, and whole organisms from stress and injury. Enhanced expression of heat shock protein (HSP) has been hypothesized to be responsible for this protection. To date, there are no clear mechanistic data confirming this relationship. This study tested the hypothesis that GLN-mediated activation of the HSP pathway via heat shock factor-1 (HSF-1) is responsible for cellular protection. Wild-type HSF-1 (HSF-1+/+) and knockout (HSF-1−/−) mouse fibroblasts were used in all experiments. Cells were treated with GLN concentrations ranging from 0 to 16 mM and exposed to heat stress injury in a concurrent treatment model. Cell viability was assayed with phenazine methosulfate plus tetrazolium salt, HSP-70, HSP-25, and nuclear HSF-1 expression via Western blot analysis, and HSF-1/heat shock element (HSE) binding via EMSA. GLN significantly attenuated heat-stress induced cell death in HSF-1+/+ cells in a dose-dependent manner; however, the survival benefit of GLN was lost in HSF-1−/− cells. GLN led to a dose-dependent increase in HSP-70 and HSP-25 expression after heat stress. No inducible HSP expression was observed in HSF-1−/− cells. GLN increased unphosphorylated HSF-1 in the nucleus before heat stress. This was accompanied by a GLN-mediated increase in HSF-1/HSE binding and nuclear content of phosphorylated HSF-1 after heat stress. This is the first demonstration that GLN-mediated cellular protection after heat-stress injury is related to HSF-1 expression and cellular capacity to activate an HSP response. Furthermore, the mechanism of GLN-mediated protection against injury appears to involve an increase in nuclear HSF-1 content before stress and increased HSF-1 promoter binding and phosphorylation.


1999 ◽  
Vol 112 (16) ◽  
pp. 2765-2774 ◽  
Author(s):  
P.A. Mercier ◽  
N.A. Winegarden ◽  
J.T. Westwood

The induction of the heat shock genes in eukaryotes by heat and other forms of stress is mediated by a transcription factor known as heat shock factor 1 (HSF1). HSF1 is present in unstressed metazoan cells as a monomer with low affinity for DNA, and upon exposure to stress it is converted to an ‘active’ homotrimer that binds the promoters of heat shock genes with high affinity and induces their transcription. The conversion of HSF1 to its active form is hypothesized to be a multistep process involving physical changes in the HSF1 molecule and the possible translocation of HSF1 from the cytoplasm to the nucleus. While all studies to date have found active HSF1 to be a nuclear protein, there have been conflicting reports on whether the inactive form of HSF is predominantly a cytoplasmic or nuclear protein. In this study, we have made antibodies against human HSF1 and have reexamined its localization in unstressed and heat-shocked human HeLa and A549 cells, and in green monkey Vero cells. Biochemical fractionation of heat-shocked HeLa cells followed by western blot analysis showed that HSF1 was mostly found in the nuclear fraction. In extracts made from unshocked cells, HSF1 was predominantly found in the cytoplasmic fraction using one fractionation procedure, but was distributed approximately equally between the cytoplasmic and nuclear fractions when a different procedure was used. Immunofluorescence microscopy revealed that HSF1 was predominantly a nuclear protein in both heat shocked and unstressed cells. Quantification of HSF1 staining showed that approximately 80% of HSF1 was present in the nucleus both before and after heat stress. These results suggest that HSF1 is predominantly a nuclear protein prior to being exposed to stress, but has low affinity for the nucleus and is easily extracted using most biochemical fractionation procedures. These results also imply that HSF1 translocation is probably not part of the multistep process in HSF1 activation for many cell types.


2008 ◽  
Vol 7 (9) ◽  
pp. 1573-1581 ◽  
Author(s):  
Seona Thompson ◽  
Nirvana J. Croft ◽  
Antonis Sotiriou ◽  
Hugh D. Piggins ◽  
Susan K. Crosthwaite

ABSTRACT Appropriate responses of organisms to heat stress are essential for their survival. In eukaryotes, adaptation to high temperatures is mediated by heat shock transcription factors (HSFs). HSFs regulate the expression of heat shock proteins, which function as molecular chaperones assisting in protein folding and stability. In many model organisms a great deal is known about the products of hsf genes. An important exception is the filamentous fungus and model eukaryote Neurospora crassa. Here we show that two Neurospora crassa genes whose protein products share similarity to known HSFs play different biological roles. We report that heat shock factor 1 (hsf1) is an essential gene and that hsf2 is required for asexual development. Conidiation may be blocked in the hsf2 knockout (hsf2 KO ) strain because HSF2 is an integral element of the conidiation pathway or because it affects the availability of protein chaperones. We report that genes expressed during conidiation, for example fluffy, conidiation-10, and repressor of conidiation-1 show wild-type levels of expression in a hsf2 KO strain. However, consistent with the lack of macroconidium development, levels of eas are much reduced. Cultures of the hsf2 KO strain along with two other aconidial strains, the fluffy and aconidial-2 strains, took longer than the wild type to recover from heat shock. Altered expression profiles of hsp90 and a putative hsp90-associated protein in the hsf2 KO strain after exposure to heat shock may in part account for its reduced ability to cope with heat stress.


Shock ◽  
2006 ◽  
Vol 25 (Supplement 1) ◽  
pp. 63
Author(s):  
P. E. Wischmeyer ◽  
A. Morrison ◽  
K. Singleton ◽  
K. Odoms ◽  
H. R. Wong

2020 ◽  
Vol 25 (1) ◽  
pp. 57-63
Author(s):  
Zamarud Shah ◽  
Safdar Hussain Shah ◽  
Gul Shad Ali ◽  
Iqbal Munir ◽  
Raham Sher Khan ◽  
...  

Molecules ◽  
2020 ◽  
Vol 25 (18) ◽  
pp. 4270
Author(s):  
Zhou Li ◽  
Weihang Zeng ◽  
Bizhen Cheng ◽  
Ting Huang ◽  
Yan Peng ◽  
...  

γ-Aminobutyric acid (GABA) participates in the regulation of adaptability to abiotic stress in plants. The objectives of this study were to investigate the effects of GABA priming on improving thermotolerance in creeping bentgrass (Agrostis stolonifera) based on analyses of physiology and proteome using iTRAQ technology. GABA-treated plants maintained significantly higher endogenous GABA content, photochemical efficiency, performance index on absorption basis, membrane stability, and osmotic adjustment (OA) than untreated plants during a prolonged period of heat stress (18 days), which indicated beneficial effects of GABA on alleviating heat damage. Protein profiles showed that plants were able to regulate some common metabolic processes including porphyrin and chlorophyll metabolism, glutathione metabolism, pyruvate metabolism, carbon fixation, and amino acid metabolism for heat acclimation. It is noteworthy that the GABA application particularly regulated arachidonic acid metabolism and phenylpropanoid biosynthesis related to better thermotolerance. In response to heat stress, the GABA priming significantly increased the abundances of Cu/ZnSOD and APX4 that were consistent with superoxide dismutase (SOD) and ascorbate peroxidase (APX) activities. The GABA-upregulated proteins in relation to antioxidant defense (Cu/ZnSOD and APX4) for the reactive oxygen species scavenging, heat shock response (HSP90, HSP70, and HSP16.9) for preventing denatured proteins aggregation, stabilizing abnormal proteins, promoting protein maturation and assembly, sugars, and amino acids metabolism (PFK5, ATP-dependent 6-phosphofructokinase 5; FK2, fructokinase 2; BFRUCT, β-fructofuranosidase; RFS2, galactinol-sucrose galactosyltransferase 2; ASN2, asparagine synthetase 2) for OA and energy metabolism, and transcription factor (C2H2 ZNF, C2H2 zinc-finger protein) for the activation of stress-defensive genes could play vital roles in establishing thermotolerance. Current findings provide an illuminating insight into the new function of GABA on enhancing adaptability to heat stress in plants.


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