Metal-responsive elements confer cadmium response in Arabidopsis

Wang, Qianqian; Gao, Ziqiang; Shi, Yang; Qi, Xiaoting

doi:10.1007/s00425-023-04093-4

Cited by 7 publications

(2 citation statements)

References 25 publications

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“…A series of plasmids related to S-HsfA2 ( 35S:S-HsfA2-Flag , 35S:S-HsfA2 L-A -Flag , and 35S:S-HsfA2-RNAi ), GUS reporter constructs [ HRE-35Sm:GUS , mHRE-35Sm:GUS, and 35Sm:GUS (Wang et al, 2023)], recombinant vectors for HSP17.6B ( 35S:HSP17.6B-Flag, HSP17.6Bp:GUS , and HSP17Bp Δ HRE:GUS ), and GFP fusion vectors ( 35S:S-HsfA2-GFP and 35S:S-HsfA4c-GFP ) were introduced into the Agrobacterium GV3101 strain, which was subsequently used to transform the Columbia wild type using the flower infiltration method. The transgenic plants used in this study were T 3 homozygous plants.…”

Section: Methodsmentioning

confidence: 99%

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Short heat shock factor A2 confers heat sensitivity inArabidopsis: Insights into heat resistance and growth balance

Chen,

Zhao,

Tao

et al. 2024

Preprint

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Cells prevent heat damage through a highly conserved canonical heat stress response (HSR) in which heat shock factors (HSFs) bind heat shock elements (HSEs) to activate heat shock proteins (HSPs). Plants generate short HSFs that originate from HSF splicing variants, but little is known about S-HSFs. Although an enhanced canonical HSR confers thermotolerance, its hyperactivation inhibits plant growth. How this process is prevented to ensure proper plant growth has not been determined. Here, we report thatArabidopsisS-HsfA2, S-HsfA4c, and S-HsfB1 confer extreme heat (45°C) sensitivity and represent new kinds of HSF with a unique truncated DNA-binding domain (tDBD) that binds a new heat-regulated element (HRE). The HRE conferred a minimal promoter response to heat and exhibited heat stress sensing and transmission patterns. We used S-HsfA2 to investigate whether and how S-HSFs prevent hyperactivation of the canonical HSR.HSP17.6B,a direct target gene of HsfA2, conferred thermotolerance, but its overexpression caused HSR hyperactivation. We revealed that S-HsfA2 alleviated this hyperactivation in two different ways. 1) S-HsfA2 negatively regulatesHSP17.6B viathe HRE-HRE-like element, thus constructing a noncanonical HSR (S-HsfA2-HRE-HSP17.6B) to antagonistically repress HsfA2-activatedHSP17.6Bexpression. 2) S-HsfA2 binds to the DBD of HsfA2 to prevent HsfA2 from binding to HSEs, eventually attenuating HsfA2-activatedHSP17.6Bpromoter activity. Overall, our findings underscore the biological importance of S-HSFs, namely, preventing plant heat tolerance hyperactivation to maintain proper growth.Graphical Abstract

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Section: Methodsmentioning

confidence: 99%

Section: Plant Transformation and Crossing 25/53mentioning

confidence: 99%