Summary: Global warming has reduced the productivity of many field‐grown crops, as the effects of high temperatures can lead to male sterility in such plants. Genetic regulation of the high temperature (HT) response in the major crop cotton is poorly understood. We determined the functionality and transcriptomes of the anthers of 218 cotton accessions grown under HT stress. By analyzing transcriptome divergence and implementing a genome‐wide association study (GWAS), we identified three thermal tolerance associated loci which contained 75 protein coding genes and 27 long noncoding RNAs, and provided expression quantitative trait loci (eQTLs) for 13 132 transcripts. A transcriptome‐wide association study (TWAS) confirmed six causal elements for the HT response (three genes overlapped with the GWAS results) which are involved in protein kinase activity. The most susceptible gene, GhHRK1, was confirmed to be a previously uncharacterized negative regulator of the HT response in both cotton and Arabidopsis. These functional variants provide a new understanding of the genetic basis for HT tolerance in male reproductive organs.

High temperature (HT) causes male sterility and decreases crop yields. Our previous works have demonstrated that sugar and auxin signaling pathways, Gossypium hirsutum Casein kinase I (GhCKI), and DNA methylation are all involved in HT-induced male sterility in cotton. However, the signaling mechanisms leading to distinct GhCKI expression patterns induced by HT between HT-tolerant and HT-sensitive cotton anthers remain largely unknown. Here, we identified a GhCKI promoter (ProGhCKI) region that functions in response to HT in anthers and found the transcription factor GhMYB4 binds to this region to act as an upstream positive regulator of GhCKI. In the tapetum of early-stage cotton anthers, upregulated expression of GhMYB4 under HT and overexpressed GhMYB4 under normal temperature both led to severe male sterility phenotypes, coupled with enhanced expression of GhCKI. We also found that GhMYB4 interacts with GhMYB66 to form a heterodimer to enhance its binding to ProGhCKI. However, GhMYB66 showed an expression pattern similar to GhMYB4 under HT but did not directly bind to ProGhCKI. Furthermore, HT reduced siRNA-mediated CHH DNA methylations in the GhMYB4 promoter, which enhanced the expression of GhMYB4 in tetrad stage anthers and promoted the formation of the GhMYB4/GhMYB66 heterodimer, which in turn elevated the transcription of GhCKI in the tapetum, leading to male sterility. Overall, we shed light on the GhMYB66–GhMYB4–GhCKI regulatory pathway in response to HT in cotton anthers.

Extreme heat driven by climate change poses a catastrophic threat to global vegetable production, undermining nutritional security because of the heightened physiological sensitivity and succulent tissues of these crops. This review synthesizes the multistage impacts of heat stress across critical developmental phases—from germination to reproduction—emphasizing morphological impairments (such as leaf wilting and floral abortion) and physiological disruptions (including photosynthetic inhibition and oxidative damage). We systematically dissect thermotolerance mechanisms in vegetables, highlighting transcriptional reprogramming by HSFs, WRKY, and NAC transcription factors; chaperone-mediated proteostasis via HSPs; epigenetic remodeling; Ca2+-ROS signaling pathways; and the role of phase separation dynamics. Importantly, we propose six strategic pathways to develop heat-resilient vegetables: harnessing natural variation through pan-genome-driven allele mining; employing biotechnological interventions such as CRISPR-mediated editing and synthetic promoters; engineering multistress tolerance by targeting conserved ‘core response’ pathways; exploiting epigenetic memory to achieve transgenerational resilience; optimizing source-sink dynamics with ‘’Climate-Responsive Carbon Optimization; and applying plant growth regulators and nanotechnology to enhance thermotolerance. Together, these strategies chart a clear roadmap for climate-smart vegetable breeding and call for interdisciplinary collaboration to translate molecular discoveries into practical breeding approaches for sustainable food systems under escalating thermal extremes.

High-temperature stress in plant stamens frequently causes male sterility, limiting crop yields. Gene duplication resulting from polyploidization offers insights into plant adaptation to environmental stress. Here, we reveal that extensive duplication of GhRALF30L , which encodes an intrinsically disordered small peptide, contributes to thermotolerance in cotton male reproductive organs. Polyploidization has driven the formation of 23 GhRALF30L genes in allotetraploid cotton, whereas only four or five homologs are identified in its two diploid ancestors. Expression and functional analyses confirm that GhRALF30L regulates thermotolerance in a dosage-dependent manner, with reduced dosage decreasing heat resistance. Under heat stress, GhRALF30L interacts with GhFERA1/GhCAPA1 and enhances their condensation at the plasma membrane, which activates heat stress responses by up-regulating the expression of heat shock factors ( HSFs ), heat shock proteins ( HSPs ), and reactive oxygen species scavenging genes. Our findings demonstrate that the GhRALF30L gene cluster, resulting from polyploidization, confers thermotolerance through facilitating the condensation of GhFERA1/GhCAPA1.

The transcription factor BRASSINAZOLE-RESISTANT 1 (BZR1) plays a crucial role not only in plant responses to various biotic and abiotic stresses but also serves a critical function in plant growth and development. In this study, we analyzed the origin and evolution of the BZR family in plants. Then, we identified nine CaBZR1 genes from the pepper pan-genome and performed bioinformatics analyses. Through the integration of transcriptome data analysis with our prior bioinformatics findings, we have identified and selected a specific member of the CaBZR1 family, CaBZR1.2, for further comprehensive investigation. We systematically investigated the biological function of CaBZR1.2 in pepper through classical reverse genetics approaches and subsequently identified proteins that interact with CaBZR1.2. After inhibiting the expression of CaBZR1.2 via virus-induced gene silencing (VIGS), the growth of pepper lateral branches was significantly suppressed, whereas heterologous overexpression of CaBZR1.2 increased lateral branch number in tomato. This result confirms the key role of CaBZR1.2 in the development of pepper lateral branches. Furthermore, protein–protein interaction assays confirmed that the Sucrose Nonfermenting 1-Related Protein Kinase 1 β subunit 2 (CaSnRK1β2) protein interacts with CaBZR1.2, with subsequent analyses revealing that these two proteins modulate pepper lateral branch development through a mutually antagonistic regulatory mechanism. This study reveals a novel mechanism by which CaBZR1.2 and CaSnRK1β2 coordinately regulate lateral branch development in pepper, providing candidate genes and a theoretical basis for the molecular breeding for pepper plant architecture.