Overexpression of SlERF3b and SlERF5 in transgenic tomato alters fruit size, number of seeds and promotes early flowering, tolerance to abiotic stress and resistance to Botrytis cinerea infection

Abstract

AbstractEthylene response factors (ERFs) are a large family of plant‐specific transcription factors that have been implicated in positively regulating stress responses. The aim of this work was to study the expression pattern of ethylene response factors SlERF1, SlERF3b and SlERF5 in Solanum lycopersicum cv. Ailsa Craig, when subjected to different stress conditions, as well as to determine the overexpression effect in transgenic tomato when exposed to abiotic and biotic stress conditions. Here we report that SlERF1, SlERF3b and SlERF5 genes are differentially upregulated in tomato wild‐type plants grown under either simulated biotic (when trehalose was applied exogenously) and abiotic stress. SlERF5 and SlERF3b are mainly induced under dehydration and salinity conditions; SlERF1 and SlERF5 are upregulated in response to exogenous trehalose, while SlERF3b is downregulated. These results suggest that SlERF3b could be involved in modulating defence responses to abiotic and biotic stresses. The overexpression of SlERF3b and SlERF5 in transgenic tomato plants promotes abiotic stress tolerance as a result of upregulating genes involved to confer stress tolerance such as P5CS and APx, triggering a major cell membrane‐mediated protection against oxidative stress and avoiding chlorophyll degradation under salinity and drought conditions. Transgenic plants overexpressing SlERF3b positively regulates fruit development, seed production and early flowering; however, germination seeds are more sensitive to osmotic stress as compared to saline stress, while SlERF5 transgenic line has better germination rate in saline stress compared to osmotic stress. On the other hand, overexpression of SlERF5 and SlERF3b plays an important role in regulating the immune response against the pathogenic fungus Botrytis cinerea, by positively regulating JA/ET signalling pathways.