scholarly journals Transcriptome Analysis Reveals Complex Defensive Mechanisms in Salt-Tolerant and Salt-Sensitive Shrub Willow Genotypes under Salinity Stress

2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Dezong Sui ◽  
Baosong Wang
Keyword(s):  
Cell Wall ◽  
Transcription Factors ◽  
Heat Shock ◽  
Salt Tolerance ◽  
Salinity Stress ◽  
Salt Tolerant ◽  
Tolerance Mechanism ◽  
Shrub Willow ◽  
Time Points ◽  
Shock Proteins

Salinity stress is one of the most devastating abiotic stresses limiting plant growth and productivity. As a moderately salt-tolerant crop, shrub willow (Salix spp.) is widely distributed over the world and can provide multiple bioenergy product and environmental benefits. To delve into the salt tolerance mechanism and screen out salt-tolerant genes, two shrub willow cultivars (a salt-sensitive genotype JW9-6 and a salt-tolerant genotype JW2372) at three time points (0, 2, and 12 h) after NaCl treatments were used for RNA sequencing. A comparative analysis between genotypes and time points showed 1,706 differentially expressed genes (DEGs), of which 1,029 and 431 DEGs were only found in the JW9-6 and JW2372, respectively. Gene Ontology (GO) and MapMan annotations suggested that many DEGs were involved in various defense-related biological pathways, including cell wall integrity, hormone signaling, antioxidant system, heat shock proteins, and transcription factors. Compared to JW9-6, JW2372 contained more DEGs involved in the maintenance of the cell wall integrity, ABA, and ethylene signal transduction pathways. In addition, more DEGs encoding heat shock proteins were found in JW2372. Instead, transcription factors including ERF, MYB, NAC, and WRKY were found to be more differentially expressed in JW9-6 under salinity stress. Furthermore, expressions of nine randomly selected DEGs were verified by qRT-PCR analysis. This study contributes in new perspicacity into underlying the salt tolerance mechanism of a shrub willow at the transcriptome level and also provides numerous salt-tolerant genes for further genetic engineering and breeding purposes in the future.

scholarly journals Arabidopsis heat shock transcription factor HSFA7b positively mediates salt stress tolerance by binding to an E-box-like motif to regulate gene expression

2019 ◽  
Vol 70 (19) ◽  
pp. 5355-5374 ◽  
Author(s):  
Dandan Zang ◽  
Jingxin Wang ◽  
Xin Zhang ◽  
Zhujun Liu ◽  
Yucheng Wang
Keyword(s):  
Gene Expression ◽  
Transcription Factors ◽  
Heat Shock ◽  
Salt Tolerance ◽  
Stress Responses ◽  
Ion Homeostasis ◽  
Cellulose Synthase ◽  
Regulate Gene Expression ◽  
E Box ◽  
Regulate Gene

Abstract Plant heat shock transcription factors (HSFs) are involved in heat and other abiotic stress responses. However, their functions in salt tolerance are little known. In this study, we characterized the function of a HSF from Arabidopsis, AtHSFA7b, in salt tolerance. AtHSFA7b is a nuclear protein with transactivation activity. ChIP-seq combined with an RNA-seq assay indicated that AtHSFA7b preferentially binds to a novel cis-acting element, termed the E-box-like motif, to regulate gene expression; it also binds to the heat shock element motif. Under salt conditions, AtHSFA7b regulates its target genes to mediate serial physiological changes, including maintaining cellular ion homeostasis, reducing water loss rate, decreasing reactive oxygen species accumulation, and adjusting osmotic potential, which ultimately leads to improved salt tolerance. Additionally, most cellulose synthase-like (CSL) and cellulose synthase (CESA) family genes were inhibited by AtHSFA7b; some of them were randomly selected for salt tolerance characterization, and they were mainly found to negatively modulate salt tolerance. By contrast, some transcription factors (TFs) were induced by AtHSFA7b; among them, we randomly identified six TFs that positively regulate salt tolerance. Thus, AtHSFA7b serves as a transactivator that positively mediates salinity tolerance mainly through binding to the E-box-like motif to regulate gene expression.

scholarly journals Transcriptome analysis of bread wheat leaves in response to salt stress

PLoS ONE ◽  
2021 ◽  
Vol 16 (7) ◽  
pp. e0254189
Author(s):  
Nazanin Amirbakhtiar ◽  
Ahmad Ismaili ◽  
Mohammad-Reza Ghaffari ◽  
Raheleh Mirdar Mansuri ◽  
Sepideh Sanjari ◽  
...  
Keyword(s):  
Salt Tolerance ◽  
Salinity Stress ◽  
Expression Patterns ◽  
Transcript Abundance ◽  
Crop Productivity ◽  
Mapk Signaling ◽  
Salt Tolerant ◽  
Illumina Hiseq ◽  
Phenylpropanoid Biosynthesis ◽  
Wheat Leaves

Salinity is one of the main abiotic stresses limiting crop productivity. In the current study, the transcriptome of wheat leaves in an Iranian salt-tolerant cultivar (Arg) was investigated in response to salinity stress to identify salinity stress-responsive genes and mechanisms. More than 114 million reads were generated from leaf tissues by the Illumina HiSeq 2500 platform. An amount of 81.9% to 85.7% of reads could be mapped to the wheat reference genome for different samples. The data analysis led to the identification of 98819 genes, including 26700 novel transcripts. A total of 4290 differentially expressed genes (DEGs) were recognized, comprising 2346 up-regulated genes and 1944 down-regulated genes. Clustering of the DEGs utilizing Kyoto Encyclopedia of Genes and Genomes (KEGG) indicated that transcripts associated with phenylpropanoid biosynthesis, transporters, transcription factors, hormone signal transduction, glycosyltransferases, exosome, and MAPK signaling might be involved in salt tolerance. The expression patterns of nine DEGs were investigated by quantitative real-time PCR in Arg and Moghan3 as the salt-tolerant and susceptible cultivars, respectively. The obtained results were consistent with changes in transcript abundance found by RNA-sequencing in the tolerant cultivar. The results presented here could be utilized for salt tolerance enhancement in wheat through genetic engineering or molecular breeding.

scholarly journals Protection against streptococcal cell wall-induced arthritis by pretreatment with the 65-kD mycobacterial heat shock protein.

1989 ◽  
Vol 170 (2) ◽  
pp. 449-466 ◽  
Author(s):  
M F van den Broek ◽  
E J Hogervorst ◽  
M C Van Bruggen ◽  
W Van Eden ◽  
R van der Zee ◽  
...  
Keyword(s):  
Cell Wall ◽  
T Cell ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
Delayed Type Hypersensitivity ◽  
Streptococcal Cell Wall ◽  
Amino Acid Homology ◽  
Lymphoid Cell Population ◽  
Shock Proteins

We report that streptococcal cell wall (SCW)-induced arthritis in rats, a T cell-dependent chronic, erosive polyarthritis, can be prevented by pretreatment of the rats with the mycobacterial 65-kD heat shock protein. This 65-kD protein shows extensive amino acid homology with prokaryotic and eukaryotic 65-kD heat shock proteins and is a ubiquitous bacterial common antigen. Both the clinical and histopathologic manifestations of the arthritis were prevented completely when rats were pretreated with 50 micrograms of 65-kD protein intraperitoneally at 35, 25, 15, or 5 d before administration of SCW. In such protected rats, SCW-specific T cell responses were suppressed, as compared with responses in arthritic rats. Pretreatment with 65-kD protein had no effect on the production of antibodies against SCW, on a nonspecific inflammatory reaction (zymosan-induced arthritis), or on general cellular immunity in vivo (delayed type hypersensitivity reaction to a nonrelated protein antigen). Furthermore, the protection against SCW arthritis was transferable by splenic T cells to naive recipients. Our data show that pretreatment with the 65-kD mycobacterial heat shock protein protects rats against a subsequent bacterium-induced arthritis. This protection is immunologically specific and resides in the lymphoid cell population.

scholarly journals Heat and water stress induce unique transcriptional signatures of heat-shock proteins and transcription factors in grapevine

2013 ◽  
Vol 14 (1) ◽  
pp. 135-148 ◽  
Author(s):  
Margarida Rocheta ◽  
Jörg D. Becker ◽  
João L. Coito ◽  
Luísa Carvalho ◽  
Sara Amâncio
Keyword(s):  
Transcription Factors ◽  
Water Stress ◽  
Heat Shock ◽  
Heat Shock Proteins ◽  
Shock Proteins

Membrane- and cell wall-associated heat shock proteins in two genotypes of barley seedlings

2000 ◽  
Vol 134 (2) ◽  
pp. 171-178 ◽  
Author(s):  
Antonella Leone ◽  
Gabriella Piro ◽  
Maria Rosaria Leucci ◽  
Giuseppe Dalessandro ◽  
Giuseppe Zacheo
Keyword(s):  
Cell Wall ◽  
Heat Shock ◽  
Heat Shock Proteins ◽  
Shock Proteins

scholarly journals Protective Effect of Post-Ischaemic Viral Delivery of Heat Shock Proteins in vivo

2008 ◽  
Vol 29 (2) ◽  
pp. 254-263 ◽  
Author(s):  
Romina A Badin ◽  
Michael Modo ◽  
Mike Cheetham ◽  
David L Thomas ◽  
David G Gadian ◽  
...  
Keyword(s):  
Heat Shock ◽  
Heat Shock Proteins ◽  
Viral Vector ◽  
Lesion Size ◽  
In Vivo Studies ◽  
Current Evidence ◽  
Time Points ◽  
Shock Proteins

Heat shock proteins (HSPs) function as molecular chaperones involved in protein folding, transport and degradation and, in addition, they can promote cell survival both in vitro and in vivo after a range of stresses. Although some in vivo studies have suggested that HSP27 and HSP70 can be neuroprotective, current evidence is limited, particularly when HSPs have been delivered after an insult. The effect of overexpressing HSPs after transient occlusion of the middle cerebral artery in rats was investigated by delivering an attenuated herpes simplex viral vector (HSV-1) engineered to express HSP27 or HSP70 30 mins after tissue reperfusion. Magnetic resonance imaging scans were used to determine lesion size and cerebral blood flow at six different time points up to 1 month after stroke. Animals underwent two sensorimotor tests at the same time points to assess the relationship between lesion size and function. Results indicate that post-ischaemic viral delivery of HSP27, but not of HSP70, caused a statistically significant reduction in lesion size and induced a significant behavioural improvement compared with controls. This is the first evidence of effective post-ischaemic gene therapy with a viral vector expressing HSP27 in an experimental model of stroke.

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