The CaM1 ‐ CBP60b ‐ MYB77 Transcriptional Cascade Regulates K ⁺ Homeostasis and Salt Tolerance in Barley

Soil salinity is a major abiotic stress that threatens global crop productivity. Calcium (Ca 2+ ) is a pivotal second messenger in plant stress signalling, but how Ca 2+ sensors such as calmodulin (CaM) transcriptionally control ion homeostasis and salt tolerance remains largely understood in crops. Here, we identified a novel calmodulin‐binding protein HvCBP60b, which is a negative regulator of salt resilience in salt‐tolerant barley. We showed that HvCBP60b interacts with Ca 2+ sensor HvCaM1 via its C‐terminal domain in a Ca 2+ ‐dependent manner. Loss of either HvCBP60b or HvCaM1 promoted the uptake of K + , increased the K + /Na + ratio, and markedly enhanced both growth performance and grain yield under salinity stress. Furthermore, HvCBP60b binds to the promoter of R2R3‐type MYB transcription factor HvMYB77 through its N‐terminal domain. HvMYB77 then transcriptionally reduces the expression of HvHAK5, a high‐affinity K + transporter essential for maintaining K + homeostasis under salinity. Mutations in HvMYB77 or HvHAK5 compromise salt tolerance, whereas the salt‐sensitive phenotype of hvhak5 is rescued in hvcbp60b‐hvhak5 double mutants. Therefore, we uncover a novel Ca 2+ ‐responsive regulatory module CaM1‐CBP60b‐MYB77‐HAK5 essential for K + homeostasis and salt tolerance in barley, highlighting new targets of Ca 2+ signalling for improving salt resilience in cereal crops.