scholarly journals Transcriptional Basis for Differential Thermosensitivity of Seedlings of Various Tomato Genotypes

Genes ◽  
2020 ◽  
Vol 11 (6) ◽  
pp. 655
Author(s):  
Yangjie Hu ◽  
Sotirios Fragkostefanakis ◽  
Enrico Schleiff ◽  
Stefan Simm

Transcriptional reprograming after the exposure of plants to elevated temperatures is a hallmark of stress response which is required for the manifestation of thermotolerance. Central transcription factors regulate the stress survival and recovery mechanisms and many of the core responses controlled by these factors are well described. In turn, pathways and specific genes contributing to variations in the thermotolerance capacity even among closely related plant genotypes are not well defined. A seedling-based assay was developed to directly compare the growth and transcriptome response to heat stress in four tomato genotypes with contrasting thermotolerance. The conserved and the genotype-specific alterations of mRNA abundance in response to heat stress were monitored after exposure to three different temperatures. The transcripts of the majority of genes behave similarly in all genotypes, including the majority of heat stress transcription factors and heat shock proteins, but also genes involved in photosynthesis and mitochondrial ATP production. In turn, genes involved in hormone and RNA-based regulation, such as auxin- and ethylene-related genes, or transcription factors like HsfA6b, show a differential regulation that associates with the thermotolerance pattern. Our results provide an inventory of genes likely involved in core and genotype-dependent heat stress response mechanisms with putative role in thermotolerance in tomato seedlings.

2007 ◽  
Vol 189 (24) ◽  
pp. 8818-8827 ◽  
Author(s):  
Diana L. Williams ◽  
Tana L. Pittman ◽  
Mike Deshotel ◽  
Sandra Oby-Robinson ◽  
Issar Smith ◽  
...  

ABSTRACT Mycobacterium leprae, a major human pathogen, grows poorly at 37°C. The basis for its inability to survive at elevated temperatures was investigated. We determined that M. leprae lacks a protective heat shock response as a result of the lack of transcriptional induction of the alternative sigma factor genes sigE and sigB and the major heat shock operons, HSP70 and HSP60, even though heat shock promoters and regulatory circuits for these genes appear to be intact. M. leprae sigE was found to be capable of complementing the defective heat shock response of mycobacterial sigE knockout mutants only in the presence of a functional mycobacterial sigH, which orchestrates the mycobacterial heat shock response. Since the sigH of M. leprae is a pseudogene, these data support the conclusion that a key aspect of the defective heat shock response in M. leprae is the absence of a functional sigH. In addition, 68% of the genes induced during heat shock in M. tuberculosis were shown to be either absent from the M. leprae genome or were present as pseudogenes. Among these is the hsp/acr2 gene, whose product is essential for M. tuberculosis survival during heat shock. Taken together, these results suggest that the reduced ability of M. leprae to survive at elevated temperatures results from the lack of a functional transcriptional response to heat shock and the absence of a full repertoire of heat stress response genes, including sigH.


1998 ◽  
Vol 23 (4) ◽  
pp. 313-329 ◽  
Author(s):  
Klaus-Dieter Scharf ◽  
Ingo Höhfeld ◽  
Lutz Nover

2004 ◽  
Vol 29 (4) ◽  
pp. 471-487 ◽  
Author(s):  
Sanjeev Kumar Baniwal ◽  
Kapil Bharti ◽  
Kwan Yu Chan ◽  
Markus Fauth ◽  
Arnab Ganguli ◽  
...  

2021 ◽  
Author(s):  
Sheila A Kitchen ◽  
Duo Jiang ◽  
Saki Harii ◽  
Noriyuki Satoh ◽  
Virginia M Weis ◽  
...  

The endosymbiosis between most corals and their photosynthetic dinoflagellate partners begins early in the host life history, when corals are larvae or juvenile polyps. The capacity of coral larvae to buffer climate-induced stress while in the process of symbiont acquisition could come with physiological trade-offs that alter larval behavior, development, settlement and survivorship. Here we examined the joint effects of thermal stress and symbiosis onset on colonization dynamics, survival, metamorphosis and host gene expression of Acropora digitifera larvae. We found that thermal stress decreased symbiont colonization of hosts by 50% and symbiont density by 98.5% over two weeks. Temperature and colonization also influenced larval survival and metamorphosis in an additive manner, where colonized larvae fared worse or prematurely metamorphosed more often than non-colonized larvae under thermal stress. Transcriptomic responses to colonization and thermal stress treatments were largely independent, while the interaction of these treatments revealed contrasting expression profiles of genes that function in the stress response, immunity, inflammation and cell cycle regulation. The combined treatment either canceled or lowered the magnitude of expression of heat-stress responsive genes in the presence of symbionts, revealing a physiological cost to acquiring symbionts at the larval stage with elevated temperatures. In addition, host immune suppression, a hallmark of symbiosis onset under ambient temperature, turned to immune activation under heat stress. Thus, by integrating the physical environment and biotic pressures that mediate pre-settlement event in corals, our results suggest that colonization may hinder larval survival and recruitment creating isolated, genetically similar populations under projected climate scenarios.


2021 ◽  
Vol 22 (2) ◽  
pp. 948
Author(s):  
Zhaoxia Li ◽  
Stephen H. Howell

High temperatures causing heat stress disturb cellular homeostasis and impede growth and development in plants. Extensive agricultural losses are attributed to heat stress, often in combination with other stresses. Plants have evolved a variety of responses to heat stress to minimize damage and to protect themselves from further stress. A narrow temperature window separates growth from heat stress, and the range of temperatures conferring optimal growth often overlap with those producing heat stress. Heat stress induces a cytoplasmic heat stress response (HSR) in which heat shock transcription factors (HSFs) activate a constellation of genes encoding heat shock proteins (HSPs). Heat stress also induces the endoplasmic reticulum (ER)-localized unfolded protein response (UPR), which activates transcription factors that upregulate a different family of stress response genes. Heat stress also activates hormone responses and alternative RNA splicing, all of which may contribute to thermotolerance. Heat stress is often studied by subjecting plants to step increases in temperatures; however, more recent studies have demonstrated that heat shock responses occur under simulated field conditions in which temperatures are slowly ramped up to more moderate temperatures. Heat stress responses, assessed at a molecular level, could be used as traits for plant breeders to select for thermotolerance.


2020 ◽  
Vol 71 (6) ◽  
pp. 1782-1791 ◽  
Author(s):  
Fabiola Jaimes-Miranda ◽  
Ricardo A Chávez Montes

Abstract The Multiprotein Bridging Factor 1 (MBF1) proteins are transcription co-factors whose molecular function is to form a bridge between transcription factors and the basal machinery of transcription. MBF1s are present in most archaea and all eukaryotes, and numerous reports show that they are involved in developmental processes and in stress responses. In this review we summarize almost three decades of research on the plant MBF1 family, which has mainly focused on their role in abiotic stress responses, in particular the heat stress response. However, despite the amount of information available, there are still many questions that remain about how plant MBF1 genes, transcripts, and proteins respond to stress, and how they in turn modulate stress response transcriptional pathways.


2019 ◽  
Vol 20 (22) ◽  
pp. 5603 ◽  
Author(s):  
Dong Xue ◽  
Wenzheng Liu ◽  
Yun Chen ◽  
Yingying Liu ◽  
Jiahui Han ◽  
...  

Deinococcus radiodurans is best known for its extraordinary resistance to diverse environmental stress factors, such as ionizing radiation, ultraviolet (UV) irradiation, desiccation, oxidation, and high temperatures. The heat response of this bacterium is considered to be due to a classical, stress-induced regulatory system that is characterized by extensive transcriptional reprogramming. In this study, we investigated the key functional genes involved in heat stress that were expressed and accumulated in cells (R48) following heat treatment at 48 °C for 2 h. Considering that protein degradation is a time-consuming bioprocess, we predicted that to maintain cellular homeostasis, the expression of the key functional proteins would be significantly decreased in cells (RH) that had partly recovered from heat stress relative to their expression in cells (R30) grown under control conditions. Comparative transcriptomics identified 15 genes that were significantly downregulated in RH relative to R30, seven of which had previously been characterized to be heat shock proteins. Among these genes, three hypothetical genes (dr_0127, dr_1083, and dr_1325) are highly likely to be involved in response to heat stress. Survival analysis of mutant strains lacking DR_0127 (a DNA-binding protein), DR_1325 (an endopeptidase-like protein), and DR_1083 (a hypothetical protein) showed a reduction in heat tolerance compared to the wild-type strain. These results suggest that DR_0127, DR_1083, and DR_1325 might play roles in the heat stress response. Overall, the results of this study provide deeper insights into the transcriptional regulation of the heat response in D. radiodurans.


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