Abstract:High salinity in agricultural lands is one of the predominant issues limiting agricultural yields. Plants have developed several mechanisms to withstand salinity stress, but the mechanisms are not effective enough for most crops to prevent and persist the salinity stress. Plant salt tolerance pathways involve membrane proteins that have a crucial role in sensing and mitigating salinity stress. Due to a strategic location interfacing two distinct cellular environments, membrane proteins can be considered checkp… Show more
“…Simulation data suggesting a steady shift of the active site loop towards the PPI domain and the 20 GTFA 23 manifests the autoinhibition mechanism. Membrane transporters and protein-lipid interaction in membrane is suggested to be one of the pivotal phenomena during salinity stress in plants [3,13]. CIPKs activating ions transporting membrane proteins must be membrane proximal phenomena.…”
Calcium-dependent signaling in plants is responsible for several major cellular events, including the activation of the salinity-responsive pathways. Calcium binds to calcineurin B-like protein (CBL), and the CBL-Ca2+ binds to CBL-interacting protein kinase (CIPK). The CBL-CIPK complex enhances the CIPK interaction with an upstream kinase. The upstream kinase phosphorylates CIPK that, in turn, phosphorylates membrane transporters. Targeted membrane transporter phosphorylation influences its activity and kick-starts many downstream functions, such as balancing the cytosolic Na+-to-K+ ratio. The CBL-CIPK interaction is pivotal for Ca2+-dependent salinity stress signaling. The plant contains multiple CBL and CIPK genes coded in their genomes. Hence, different yet specific combinations of CBL and CIPK are responsible for targeting particular ion transporters. Here, we present the computationally predicted structures of autoinhibited CIPK24 and CIPK24-CBL4 complex. The models are supported by the available structural and functional data. Models are energy-minimized and subjected to molecular dynamics (MD) simulations. MD simulations enabled us to predict the importance of conserved residues of the proteins. Finally, the work is extended to predict the CIPK24-CBL4 complex with the upstream kinase GIRK2. MD simulation on the ternary complex structure enabled us to identify the critical CIPK24-GIRK2 interactions. Together, these data could be used to engineer the CBL-CIPK interaction network for developing salt tolerance in crops.
“…Simulation data suggesting a steady shift of the active site loop towards the PPI domain and the 20 GTFA 23 manifests the autoinhibition mechanism. Membrane transporters and protein-lipid interaction in membrane is suggested to be one of the pivotal phenomena during salinity stress in plants [3,13]. CIPKs activating ions transporting membrane proteins must be membrane proximal phenomena.…”
Calcium-dependent signaling in plants is responsible for several major cellular events, including the activation of the salinity-responsive pathways. Calcium binds to calcineurin B-like protein (CBL), and the CBL-Ca2+ binds to CBL-interacting protein kinase (CIPK). The CBL-CIPK complex enhances the CIPK interaction with an upstream kinase. The upstream kinase phosphorylates CIPK that, in turn, phosphorylates membrane transporters. Targeted membrane transporter phosphorylation influences its activity and kick-starts many downstream functions, such as balancing the cytosolic Na+-to-K+ ratio. The CBL-CIPK interaction is pivotal for Ca2+-dependent salinity stress signaling. The plant contains multiple CBL and CIPK genes coded in their genomes. Hence, different yet specific combinations of CBL and CIPK are responsible for targeting particular ion transporters. Here, we present the computationally predicted structures of autoinhibited CIPK24 and CIPK24-CBL4 complex. The models are supported by the available structural and functional data. Models are energy-minimized and subjected to molecular dynamics (MD) simulations. MD simulations enabled us to predict the importance of conserved residues of the proteins. Finally, the work is extended to predict the CIPK24-CBL4 complex with the upstream kinase GIRK2. MD simulation on the ternary complex structure enabled us to identify the critical CIPK24-GIRK2 interactions. Together, these data could be used to engineer the CBL-CIPK interaction network for developing salt tolerance in crops.
The negative impacts of soil salinization on ion homeostasis provide a significant global barrier to agricultural production and development. Plant physiology and biochemistry are severely affected by primary and secondary NaCl stress impacts, which damage cellular integrity, impair water uptake, and trigger physiological drought. Determining how transcriptional factors (TFs) and hormone networks are regulated in plants in response to salt stress is necessary for developing crops that tolerate salt. This study investigates the complex mechanisms of several significant TF families that influence plant responses to salt stress, involving AP2/ERF, bZIP, NAC, MYB, and WRKY. It demonstrates how these transcription factors (TFs) help plants respond to the detrimental effects of salinity by modulating gene expression through mechanisms including hormone signaling, osmotic stress pathway activation, and ion homeostasis. Additionally, it explores the hormonal imbalances triggered by salt stress, which entail complex interactions among phytohormones like jasmonic acid (JA), salicylic acid (SA), and abscisic acid (ABA) within the hormonal regulatory networks. This review highlights the regulatory role of key transcription factors in salt-stress response, and their interaction with plant hormones is crucial for developing genome-edited crops that can enhance agricultural sustainability and address global food security challenges.
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