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Claim · model-written summary
Mutations in HvMYB77 or HvHAK5 compromise salt tolerance.
- Taxon
- Barley
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Hordeum vulgaret0 - Treatment
- Mutations in HvMYB77 or HvHAK5e0
- Gene
- HvMYB77 or HvHAK5e0
- Outcome
- salt tolerancee0
- Direction
- compromisee0
Not reportedComparator
Verbatim
t0“Barley”
e0“Mutations in HvMYB77 or HvHAK5 compromise salt tolerance”
Title
Yunfeng Xu; Haoran Sun; Lijun Liu; et al. Plant Biotechnology Journal 2026. doi:10.1111/pbi.70693
Other claims from this paper (8)
- Observation HvCBP60b, a calmodulin-binding protein, was identified as a negative regulator of salt resilience in salt-tolerant barley.
- Observation HvCBP60b interacts with the Ca2+ sensor HvCaM1 via its C-terminal domain in a Ca2+-dependent manner.
- Intervention effect Loss of either HvCBP60b or HvCaM1 promoted K+ uptake and increased the K+/Na+ ratio.
- Intervention effect Loss of either HvCBP60b or HvCaM1 markedly enhanced growth performance and grain yield under salinity stress.
- Observation HvCBP60b binds to the promoter of the R2R3-type MYB transcription factor HvMYB77 through its N-terminal domain.
- Observation HvMYB77 transcriptionally reduces the expression of the high-affinity K+ transporter gene HvHAK5.
- Observation The salt-sensitive phenotype of hvhak5 is rescued in hvcbp60b-hvhak5 double mutants.
- Mechanism The CaM1-CBP60b-MYB77-HAK5 Ca2+-responsive regulatory module is proposed to be essential for K+ homeostasis and salt tolerance in barley.