Overexpression of Rice Metacaspase, <em>OsMC4</em>, Increases Endoplasmic Reticulum Stress Tolerance in Transgenic Rice Calli

Abstract

Endoplasmic reticulum (ER) is an important organelle responsible as protein synthesis regulator in plant. High salinity can also lead to the activation of ER stress, caused by the accumulation of misfolded protein. This could lead to a stress response mechanism, unfolded protein response (UPR). Failure of UPR to reverse the effect of protein misfolding will activate Programmed Cell Death (PCD). Metacaspase genes regulate programmed cell death (PCD) in plants. The present study was focused on comprehensive gene analyses of the expression patterns of type II rice metacaspase (OsMC) genes in response to the endoplasmic reticulum (ER) and salinity stress in rice leaf and OsMC4 in callus. A strong evidence of unfolded protein response (UPR) during tolerance to both ER and salinity stress was found in the present study. Overexpression of OsMC4 in rice callus as a fusion protein with TagRFP and controlled by the CaMV35 promoter caused major changes in the expression of the stress ER-marker genes, protein disulfide isomerase (PDI) and Binding immunoglobulin Protein (BiP), and OsMC4 in overexpressing calli. These expression analyses of the OsMC family provide valuable information for further functional studies on the biological roles of OsMCs in PCD related to ER and salinity stress responses.

A GBS-based genome-wide association study reveals the genetic basis of salinity tolerance at the seedling stage in bread wheat (Triticum aestivum L.)

“…The UPR mechanism reverses misfolded proteins. UPR failure activates programmed cell death ( Yusof et al, 2021 ). Metacaspase genes are key regulators of programmed cell death and might be the cardinal components of the saline stress pathway.…”