Molecular Analysis of Rice CIPKs Involved in Both Biotic and Abiotic Stress Responses

Plant calcineurin B-like （CBL） proteins have been proposed as important Ca2＋ sensors and specifically interact with CBL-interacting protein kinases （CIPKs） in plant-specific calcium signaling. Here, we identified and isolated 15 CIPK genes in a japonica rice variety Nipponbare based on the predicted sequences of rice CIPK gene family. Gene structure analysis showed that these 15 genes were divided into intron-less and intron-rich groups, and OsCIPK3 and OsCIPK24 exhibited alternative splicing in their mature process. The phylogenetic analyses indicated that rice CIPKs shared an ancestor with Arabidopsis and poplar CIPKs. Analyses of gene expression showed that these OsCIPK genes were differentially induced by biotic stresses such as bacterial blight and abiotic stresses （heavy metal such as Hg2＋, high salinity, cold and ABA）. Interestingly, five OsCIPK genes, OsCIPK1, 2, 10, 11 and 12, were transcriptionally up-regulated after bacterial blight infection whereas four OsCIPK genes, OsCIPK2, 10, 11 and 14, were induced by all treatments, indicating that some of OsCIPK genes are involved in multiple stress response pathways in plants. Our finding suggests that CIPKs play a key role in both biotic and abiotic stress responses.

Axonal growth inhibitors and their receptors in spinal cord injury:from biology to clinical translation

Axonal growth inhibitors are released during traumatic injuries to the adult mammalian central nervous system, including after spinal cord injury. These molecules accumulate at the injury site and form a highly inhibitory environment for axonal regeneration. Among these inhibitory molecules, myelinassociated inhibitors, including neurite outgrowth inhibitor A, oligodendrocyte myelin glycoprotein, myelin-associated glycoprotein, chondroitin sulfate proteoglycans and repulsive guidance molecule A are of particular importance. Due to their inhibitory nature, they represent exciting molecular targets to study axonal inhibition and regeneration after central injuries. These molecules are mainly produced by neurons, oligodendrocytes, and astrocytes within the scar and in its immediate vicinity. They exert their effects by binding to specific receptors, localized in the membranes of neurons. Receptors for these inhibitory cues include Nogo receptor 1, leucine-rich repeat, and Ig domain containing 1 and p75 neurotrophin receptor/tumor necrosis factor receptor superfamily member 19(that form a receptor complex that binds all myelin-associated inhibitors), and also paired immunoglobulin-like receptor B. Chondroitin sulfate proteoglycans and repulsive guidance molecule A bind to Nogo receptor 1, Nogo receptor 3, receptor protein tyrosine phosphatase σ and leucocyte common antigen related phosphatase, and neogenin, respectively. Once activated, these receptors initiate downstream signaling pathways, the most common amongst them being the Rho A/ROCK signaling pathway. These signaling cascades result in actin depolymerization, neurite outgrowth inhibition, and failure to regenerate after spinal cord injury. Currently, there are no approved pharmacological treatments to overcome spinal cord injuries other than physical rehabilitation and management of the array of symptoms brought on by spinal cord injuries. However, several novel therapies aiming to modulate these inhibitory proteins and/or their receptors are under investigation in ongoing clinical trials. Investigation has also been demonstrating that combinatorial therapies of growth inhibitors with other therapies, such as growth factors or stem-cell therapies, produce stronger results and their potential application in the clinics opens new venues in spinal cord injury treatment.