Plasma membrane‐localized Hsp40/DNAJ chaperone protein facilitates OsSUVH7‐OsBAG4‐OsMYB106 transcriptional complex formation for OsHKT1;5 activation.

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 membrane‐localized 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, OsDNAJ15‐overexpression 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. [ABSTRACT FROM AUTHOR]