• Book : 202()
• Pub. Date : 2025
• Page : pp.110608
• Keyword :

• Book : 202()
• Pub. Date : 2025
• Page : pp.110617
• Keyword :

• Book : 217()
• Pub. Date : 2025
• Page : pp.111633
• Keyword :

• Book : 180()
• Pub. Date : 2025
• Page : pp.105587
• Keyword :

• Book : 180()
• Pub. Date : 2025
• Page : pp.105582
• Keyword :

ABSTRACT

Drought is an important abiotic factor constricting crop production globally. Although the roles of JAZ proteins in regulating jasmonic acid signalling and plant responses to environmental stress are well documented, their specific functions and underlying mechanisms remain little known. In this study, JAZ proteins in barley were thoroughly analyzed, revealing a total of 11 members classified into three phylogenetic subgroups. HvJAZ2, based on its distinct expression patterns, is considered a key candidate gene for regulating drought tolerance in barley. Using the HvJAZ2 knockout mutants, we revealed that the gene negatively regulates drought tolerance by inhibiting barley root growth. Notably, the jaz2 mutants upregulated the expression of root development genes, including SHR1, PLT1, PLT2 and PLT6. plt2 and plt1/plt2 mutants exhibited suppressed root development and reduced drought tolerance. Analysis of interactions between HvJAZ2 and other proteins showed that HvJAZ2 does not directly interact with HvPLT1/2/6, but interacts with some other proteins. BIFC and LCA assays further confirmed the nuclear interaction between HvJAZ2 and HvMYC2. Y1H and Dual‐Luciferase experiments demonstrated that HvMYC2 can bind to and activate the HvPLT2 promoter. In summary, HvJAZ2 negatively regulates root development and drought tolerance in barley by suppressing HvPLT2 expression through interacting with HvMYC2.

Summary statement

Drought is a major abiotic factor limiting crop production globally.

This study found HvJAZ2 negatively regulates drought tolerance in barley (Hordeum vulgare L.) by suppressing HvPLT2 expression through interacting with HvMYC2, which is potentially useful for improving barley's drought tolerance.

• Book : 48(1)
• Pub. Date : 2025
• Page : pp.699-710
• Keyword :

• Book : 605()
• Pub. Date : 2025
• Page : pp.155562
• Keyword :

• Book : 860()
• Pub. Date : 2025
• Page : pp.139186
• Keyword :

ABSTRACT

Although WRKY transcription factors play crucial roles in plant responses to high‐temperature stress, little is known about Group IIb WRKY family members. Here, we identified the WRKY‐IIb protein PlWRKY47 from herbaceous peony (Paeonia lactiflora Pall.), which functioned as a nuclear‐localized transcriptional activator. The expression level of PlWRKY47 was positively correlated with high‐temperature tolerance. Silencing of PlWRKY47 in P. lactiflora resulted in the decreased tolerance to high‐temperature stress by accumulating reactive oxygen species (ROS). Overexpression of PlWRKY47 improved plant high‐temperature tolerance through decreasing ROS accumulation. Moreover, PlWRKY47 directly bound to the promoter of cytosolic glyceraldehyde‐3‐phosphate dehydrogenase 2 (PlGAPC2) gene and activated its transcription. PlGAPC2 was also positively regulated high‐temperature tolerance in P. lactiflora by increasing NAD⁺ content to inhibit ROS generation. Additionally, PlWRKY47 physically interacted with itself to form a homodimer, and PlWRKY47 could also interact with one Group IIb WRKY family member PlWRKY72 to form a heterodimer, they all promoted PlWRKY47 to bind to and activate PlGAPC2. These data support that the PlWRKY47‐PlWRKY47 homodimer and PlWRKY72‐PlWRKY47 heterodimer can directly activate PlGAPC2 expression to improve high‐temperature tolerance by inhibiting ROS generation in P. lactiflora. These results will provide important insights into the plant high‐temperature stress response by WRKY‐IIb transcription factors.

Summary statement

Herbaceous peony PlWRKY47‐PlWRKY47 homodimer and PlWRKY72‐PlWRKY47 heterodimer can directly activate the expression of cytosolic glyceraldehyde‐3‐phosphate dehydrogenase 2 gene to improve high‐temperature tolerance by increasing NAD⁺ content to inhibit ROS generation.

• Book : 48(1)
• Pub. Date : 2025
• Page : pp.226-243
• Keyword :

• Book : 229()
• Pub. Date : 2025
• Page : pp.112492
• Keyword :