Knockdown of NON-YELLOW COLORING 1 (NYC1)-like gene or chlorophyllin application enhanced chlorophyll accumulation with antioxidant roles in suppressing heat-induced leaf senescence in perennial ryegrass.

Abstract

Loss of chlorophyll (Chl) and oxidative damages co-occur during heat-induced leaf senescence. This study aimed to determine the functions of Chl catabolic gene, NON-YELLOW COLORING 1 (NYC1)-like (NOL) in regulating heat-induced leaf senescence and to characterize antioxidant roles of a Chl derivative, sodium copper chlorophyllin (SCC), in suppressing heat-induced leaf senescence. In two separate experiments, one by comparing NOL RNAi transgenic and wild-type plants, and the other by analyzing the effects of sodium copper chlorophyllin (SCC, 1\xa0mM) treatment, perennial ryegrass (Lolium perenne) were exposed to heat stress (38/35 oC, day/night) or optimal temperature (25/20 oC). Results showed that both knockdown of LpNOL and application of SCC suppressed heat-induced leaf senescence, as manifested by increased Chl content, reduced electrolyte leakage, and down-regulation of Chl-catabolic genes and senescence-related genes, as well as enhanced antioxidant capacity in the peroxidase (POD) pathway for H2O2 scavenging. Ex vivo SCC incubation protected membranes from H2O2 damage onto mesophyll protoplasts of perennial ryegrass. The suppression of leaf senescence by knockdown of NOL or chlorophyllin application was associated with enhanced chlorophyll accumulation playing antioxidant roles in protecting leaves from heat-induced oxidative damages.