Summary Reactive oxygen species (ROS) act as important secondary messengers in abscisic acid (ABA) signaling and induce stomatal closure under dehydration stress. The breast cancer susceptibility gene 1 (BRCA1), an important tumor suppressor in animals, functions primarily in the maintenance of genome integrity in animals and plants. However, whether and how the plant BRCA1 regulates intracellular ROS homeostasis in guard cells under dehydration stress remains unknown. Here, we found that Arabidopsis atbrca1 loss‐of‐function mutants showed dehydration stress tolerance. This stress tolerant phenotype of atbrca1 was a result of ABA‐ and ROS‐induced stomatal closure, which was enhanced in atbrca1 mutants compared with the wild‐type. AtBRCA1 downregulated the expression of ROS‐responsive and marker genes. Notably, these genes were also the targets of the AP2/ERF transcriptional activator RRTF1/ERF109. Under normal conditions, AtBRCA1 physically interacted with RRTF1 and inhibited its binding to the GCC‐box‐like sequence in target gene promoters. Under dehydration stress, the expression of AtBRCA1 was dramatically reduced and that of RRTF1 was activated, thus inducing the expression of ROS‐responsive genes. Overall, our study reveals a novel molecular function of AtBRCA1 in the transcriptional regulation of intracellular ROS homeostasis under dehydration stress.

DNA methylation and histone modification are evolutionarily conserved epigenetic modifications that are crucial for the expression regulation of abiotic stress-responsive genes in plants. Dynamic changes in gene expression levels can result from changes in DNA methylation and histone modifications. In the last two

The salinization of irrigated land affects agricultural productivity. HIGH-AFFINITY POTASSIUM (K + ) TRANSPORTER 1;5 (OsHKT1;5)-dependent sodium (Na + ) transport is a key salt tolerance mechanism during rice growth and development. Using a previously generated high-throughput activation tagging-based T-DNA insertion mutant pool, we isolated a mutant exhibiting salt stress-sensitive phenotype, caused by a reduction in OsHKT1;5 transcripts. The salt stress-sensitive phenotype of this mutant results from the loss of function of OsDNAJ15, which encodes plasma membranelocalized heat shock protein 40 (Hsp40). osdnaj15 loss-of-function mutants show decreased plant height, increased leaf angle, and reduced grain number caused by shorter panicle length and fewer branches. On the other h`and, OsDNAJ15overexpression plants showed salt stress-tolerant phenotypes. Intriguingly, salt stress facilitates the nuclear relocation of OsDNAJ15 so that it can interact with OsBAG4, and OsDNAJ15 and OsBAG4 synergistically facilitate the DNA-binding activity of OsMYB106 to positively regulate the expression of OsHKT1;5. Overall, our results reveal a novel function of plasma membrane-localized Hsp40 protein in modulating, alongside chaperon regulator OsBAG4, transcriptional regulation under salinity stress tolerance.