Knock down of NON-YELLOW COLOURING 1-like gene or chlorophyllin application enhanced chlorophyll accumulation with antioxidant roles in suppressing heat-induced leaf senescence in perennial ryegrass

Loss of chlorophyll and oxidative damage co-occur during heat-induced leaf senescence. This study aimed to determine the functions of a chlorophyll catabolic gene, NON-YELLOW COLOURING 1 (NYC1)-like (NOL), in regulating heat-induced leaf senescence and to characterize antioxidant roles of a chlorophyll 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 analysing the effects of SCC treatment, perennial ryegrass (Lolium perenne) was exposed to heat stress (38/35 degrees C, day/night) or optimal temperature (25/20 degrees C). Results showed that both knock down of LpNOL and application of SCC suppressed heat-induced leaf senescence, as manifested by increased chlorophyll content, reduced electrolyte leakage, down-regulation of chlorophyll-catabolic genes and senescence-related genes, as well as enhanced antioxidant capacity in the peroxidase pathway for H2O2 scavenging. Ex vivo SCC incubation protected membranes from H2O2 damage in mesophyll protoplasts of perennial ryegrass. The suppression of leaf senescence by knocking down NOL or chlorophyllin application was associated with enhanced chlorophyll accumulation playing antioxidant roles in protecting leaves from heat-induced oxidative damage.

Automated summary

This study found that down-regulating the chlorophyll catabolic gene NOL or applying sodium copper chlorophyllin (SCC) can suppress heat-induced leaf senescence, increase chlorophyll content, reduce electrolyte leakage, enhance antioxidant capacity, and protect leaves from oxidative damage caused by heat.