- Information
- Symbol: OsCPK4
- MSU: LOC_Os02g03410
- RAPdb: Os02g0126400
- Publication
- Overexpression of a Calcium-Dependent Protein Kinase Confers Salt and Drought Tolerance in Rice by Preventing Membrane Lipid Peroxidation., 2014, Plant Physiol.
- Enhancing blast disease resistance by overexpression of the calcium-dependent protein kinase OsCPK4 in rice., 2015, Plant Biotechnol J.
- The kinase OsCPK4 regulates a buffering mechanism that fine-tunes innate immunity., 2017, Plant Physiol.
- Conserved Degradation of Orthologous RLCKs Regulates Immune Homeostasis., 2018, Trends Plant Sci.
-
Genbank accession number
- Key message
- A significant number of genes involved in lipid metabolism and protection against oxidative stress appear to be up-regulated by OsCPK4 in roots of overexpressor plants
- Taken together, our data show that OsCPK4 functions as a positive regulator of the salt and drought stress responses in rice via the protection of cellular membranes from stress-induced oxidative damage
- Meanwhile, OsCPK4 overexpression has no effect on the expression of well-characterized abiotic stress-associated transcriptional regulatory networks (i
- Overexpression of OsCPK4 in rice plants significantly enhances tolerance to salt and drought stress
- Compared with control plants, OsCPK4 overexpressor plants exhibit stronger water-holding capability and reduced levels of membrane lipid peroxidation and electrolyte leakage under drought or salt stress conditions
- Moreover, a plasma membrane localization of OsCPK4 was observed by transient expression assays of green fluorescent protein-tagged OsCPK4 in onion (Allium cepa) epidermal cells
- Here, we report that OsCPK4 expression is induced by high salinity, drought, and the phytohormone abscisic acid
- Also, salt-treated OsCPK4 seedlings accumulate less Na(+) in their roots
- Enhancing blast disease resistance by overexpression of the calcium-dependent protein kinase OsCPK4 in rice.
- It shows that overexpression of OsCPK4 gene in rice plants enhances resistance to blast disease by preventing fungal penetration
- Altogether, our findings indicate that OsCPK4 is a potential molecular target to improve not only abiotic stress tolerance, but also blast disease resistance of rice crops
- Given that OsCPK4 overexpression was known to confer also salt and drought tolerance in rice, the results reported in this article demonstrate that OsCPK4 acts as a convergence component that positively modulates both biotic and abiotic signalling pathways
- OsCPK4 overexpression leads also to constitutive increased content of the glycosylated salicylic acid hormone in leaves without compromising rice yield
- In this work, the isoform OsCPK4 of the rice calcium-dependent protein kinase family is reported as a regulator of rice immunity to blast fungal infection
- The constitutive accumulation of OsCPK4 protein prepares rice plants for a rapid and potentiated defence response, including the production of reactive oxygen species, callose deposition and defence gene expression
- The calcium-dependent protein kinase OsCPK4 has been demonstrated to play important roles in salt and drought tolerance, plant growth and development in rice
- In this study, we demonstrated that the generation of oxidative burst and pathogenesis-related gene expression triggered by microbe-associated molecular patterns (MAMPs) were significantly enhanced in the oscpk4 mutants
- These mutant lines are more resistant to bacterial blight and fungal blast diseases than the wild-type plants, indicating that OsCPK4 negatively regulates innate immunity in rice
- However, little is known on molecular mechanisms underlying OsCPK4 function in rice immunity
- These findings indicate that the kinase-inactive OsCPK4 promotes OsRLCK176 degradation and restricts plant defenses; whereas the activation of OsCPK4-OsRLCK176 phosphorylation circuit invalidates the OsRLCK176 degradation machinery and thus enhancing plant immunity
- The kinase OsCPK4 regulates a buffering mechanism that fine-tunes innate immunity.
- OsCPK4 was further identified to interact with a receptor-like cytoplasmic kinase OsRLCK176
- Moreover, the kinase activity and phosphorylation of OsCPK4 and OsRLCK176 contribute to the stability of OsRLCK176
- Connection
- OsCPK4, OsRLCK176~BML, The kinase OsCPK4 regulates a buffering mechanism that fine-tunes innate immunity., OsCPK4 was further identified to interact with a receptor-like cytoplasmic kinase OsRLCK176
- OsCPK4, OsRLCK176~BML, The kinase OsCPK4 regulates a buffering mechanism that fine-tunes innate immunity., OsRLCK176 accumulation is negatively regulated by OsCPK4
- OsCPK4, OsRLCK176~BML, The kinase OsCPK4 regulates a buffering mechanism that fine-tunes innate immunity., Interestingly, the kinase-dead OsCPK4 promotes OsRLCK176 degradation more strongly than the wild-type protein
- OsCPK4, OsRLCK176~BML, The kinase OsCPK4 regulates a buffering mechanism that fine-tunes innate immunity., OsCPK4 and OsRLCK176 mutually phosphorylate each other and form a feedback loop
- OsCPK4, OsRLCK176~BML, The kinase OsCPK4 regulates a buffering mechanism that fine-tunes innate immunity., Moreover, the kinase activity and phosphorylation of OsCPK4 and OsRLCK176 contribute to the stability of OsRLCK176
- OsCPK4, OsRLCK176~BML, The kinase OsCPK4 regulates a buffering mechanism that fine-tunes innate immunity., These findings indicate that the kinase-inactive OsCPK4 promotes OsRLCK176 degradation and restricts plant defenses; whereas the activation of OsCPK4-OsRLCK176 phosphorylation circuit invalidates the OsRLCK176 degradation machinery and thus enhancing plant immunity
- OsCPK18, OsCPK4, Fine-tuning OsCPK18/OsCPK4 activity via genome editing of phosphorylation motif improves rice yield and immunity., In this study, we found that OsCPK18 and its paralog OsCPK4 positively regulate plant height and yield-related traits
- OsCPK18, OsCPK4, Fine-tuning OsCPK18/OsCPK4 activity via genome editing of phosphorylation motif improves rice yield and immunity., In vitro and in vivo kinase assays demonstrated that OsMPK5 phosphorylates C-terminal threonine (T505) and serine (S512) residues of OsCPK18 and OsCPK4, respectively
- OsCPK18, OsCPK4, Fine-tuning OsCPK18/OsCPK4 activity via genome editing of phosphorylation motif improves rice yield and immunity., Interestingly, editing the MAPK phosphorylation motif in OsCPK18 and its paralog OsCPK4, which deprives OsMPK5-mediated phosphorylation but retains calcium-dependent activation of kinase activity, simultaneously increases rice yields and immunity
Prev Next