HOP1 and HOP2 are involved in salt tolerance by facilitating the brassinosteroid‐related nucleo‐cytoplasmic partitioning of the HSP90‐BIN2 complex

The co‐chaperone heat shock protein (HSP)70‐HSP90 organizing protein (HOP) is involved in plant thermotolerance. However, its function in plant salinity tolerance was not yet studied. We found that Arabidopsis HOP1 and HOP2 play critical roles in salt tolerance by affecting the nucleo‐cytoplasmic partitioning of HSP90 and brassinosteroid‐insensitive 2 (BIN2). A hop1/2 double mutant was hypersensitive to salt‐stress. Interestingly, this sensitivity was remedied by exogenous brassinolide application, while the application of brassinazole impeded growth of both wild‐type (WT) and hop1/2 plants under normal and salt stress conditions. This suggested that the insufficient brassinosteroid (BR) content was responsible for the salt‐sensitivity of hop1/2. After WT was transferred to salt stress conditions, HOP1/2, BIN2 and HSP90 accumulated in the nucleus, brassinazole‐resistant 1 (BZR1) was phosphorylated and accumulated in the cytoplasm, and BR content significantly increased. This initial response resulted in dephosphorylation of BZR1 and BR response. This dynamic regulation of BR content was impeded in salt‐stressed hop1/2. Thus, we propose that HOP1 and HOP2 are involved in salt tolerance by affecting BR signalling. Summary statement We found that hop1/2 showed increased sensitivity to NaCl which was remedied by the exogenous brassinolide application. Knockouts of both HSP70‐HSP90 organizing protein(HOP)1 and HOP2 led to, under NaCl stress, brassinosteroid (BR) deficiency and retarded hop1/2 growth. This study reveals a new mechanism of HOP1/2 function in BR regulation of salinity tolerance.