scholarly journals Heat Shock-Induced Resistance Against Pseudomonas syringae pv. tomato (Okabe) Young et al. via Heat Shock Transcription Factors in Tomato

Agronomy ◽  
2018 ◽  
Vol 9 (1) ◽  
pp. 2 ◽  
Author(s):  
Nur Akbar Arofatullah ◽  
Morifumi Hasegawa ◽  
Sayuri Tanabata ◽  
Isao Ogiwara ◽  
Tatsuo Sato

*Abstract: We investigated the role of heat shock transcription factors (Hsfs) during induction of defense response by heat-shock treatment (HST) in tomato. Leaf disease symptoms were significantly reduced at 12 and 24 h after HST, consistent with upregulation of pathogenesis-related (PR) genes PR1a2 and PR1b1 peaking at 24 h after treatment. These genes were upregulated at the treatment application site, but not in untreated leaves. In contrast to HST, inoculation of the first leaf induced systemic upregulation of acidic PR genes in uninoculated second leaves. Furthermore, heat shock element motifs were found in upstream regions of PR1a2, PR1b1, Chitinase 3, Chitinase 9, Glucanase A, and Glucanase B genes. Upregulation of HsfA2 and HsfB1 peaked at 6 h after HST, 6 h earlier than salicylic acid accumulation. Foliar spray of heat shock protein 90 (Hsp90) inhibitor geldanamycin (GDA) induced PR gene expression comparable to that after HST. PR gene expression and defense response against Pseudomonas syringae pv. tomato (Pst) decreased when combining HST with Hsfs inhibitor KRIBB11. The Hsfs and PR gene expression induced by heat or GDA, together with the suppression of heat shock-induced resistance (HSIR) against Pst by KRIBB11, suggested a direct contribution of Hsfs to HSIR regulation in tomato.

2019 ◽  
Vol 70 (19) ◽  
pp. 5355-5374 ◽  
Author(s):  
Dandan Zang ◽  
Jingxin Wang ◽  
Xin Zhang ◽  
Zhujun Liu ◽  
Yucheng Wang

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.


2018 ◽  
Author(s):  
Peter Chisnell ◽  
T. Richard Parenteau ◽  
Elizabeth Tank ◽  
Kaveh Ashrafi ◽  
Cynthia Kenyon

AbstractThe widely conserved heat-shock response, regulated by heat shock transcription factors, is not only essential for cellular stress resistance and adult longevity, but also for proper development. However, the genetic mechanisms by which heat-shock transcription factors regulate development are not well understood. In C. elegans, we conducted an unbiased genetic screen to identify mutations that could ameliorate the developmental arrest phenotype of a heat-shock factor mutant. Here we show that loss of the conserved translational activator rsks-1/S6-Kinase, a downstream effector of TOR kinase, can rescue the developmental-arrest phenotype of hsf-1 partial loss-of-function mutants. Unexpectedly, we show that the rescue is not likely caused by reduced translation, nor to activation of any of a variety of stress-protective genes and pathways. Our findings identify an as-yet unexplained regulatory relationship between the heat-shock transcription factor and the TOR pathway during C. elegans’ development.


2006 ◽  
Vol 405 (3) ◽  
pp. 191-195 ◽  
Author(s):  
Jacky M.K. Kwong ◽  
Maziar Lalezary ◽  
Jessica K. Nguyen ◽  
Christine Yang ◽  
Anuj Khattar ◽  
...  

Forests ◽  
2019 ◽  
Vol 10 (12) ◽  
pp. 1157 ◽  
Author(s):  
Yan Li ◽  
Wencai Yu ◽  
Yueyi Chen ◽  
Shuguang Yang ◽  
Shaohua Wu ◽  
...  

Heat-shock transcription factors (Hsfs) play a pivotal role in the response of plants to various stresses. The present study aimed to characterize the Hsf genes in the rubber tree, a primary global source of natural rubber. In this study, 30 Hsf genes were identified in the rubber tree using genome-wide analysis. They possessed a structurally conserved DNA-binding domain and an oligomerization domain. On the basis of the length of the insert region between HR-A and HR-B in the oligomerization domain, the 30 members were clustered into three classes, Classes A (18), B (10), and C (2). Members within the same class shared highly conserved gene structures and protein motifs. The background expression levels of 11 genes in cold-tolerant rubber-tree clone 93-14 were significantly higher than those in cold-sensitive rubber-tree clone Reken501, while four genes exhibited inverse expression patterns. Upon cold stress, 20 genes were significantly upregulated in 93-114. Of the upregulated genes, HbHsfA2b, HbHsfA3a, and HbHsfA7a were also significantly upregulated in three other cold-tolerant rubber-tree clones at one or more time intervals upon cold stress. Their nuclear localization was verified, and the protein–protein interaction network was predicted. This study provides a basis for dissecting Hsf function in the enhanced cold tolerance of the rubber tree.


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