Suppression of the target of rapamycin kinase accelerates tomato fruit ripening through reprogramming the transcription profile and promoting ethylene biosynthesis.

Abstract

Tomato fruit ripening is a unique process of nutritional and energy metabolism. Target of rapamycin (TOR), a conserved serine/threonine protein kinase in eukaryotes, controls cell growth and metabolism by integrating nutrient, energy, and hormone signals. However, it remains unclear whether TOR participates in the modulation of tomato fruit ripening. Here, we showed that the manipulation of SlTOR by chemical or genetic methods greatly alters the process of tomato fruit maturation. Expression pattern analysis revealed that the transcripts of SlTOR declined as fruit ripening progressed. Moreover, suppression of SlTOR by TOR inhibitor AZD8055 or knock down of its transcripts by inducible RNA interference, accelerated fruit ripening, and led to overall effects on fruit maturity, including changes in colour and metabolism, fruit softening, and expression of ripening-related genes. Genome-wide transcription analysis indicated that silencing SlTOR reprogrammed the transcript profile associated with ripening, including cell wall and phytohormone pathways, elevated the expression of ethylene biosynthetic genes, and further promoted ethylene production. In contrast, the ethylene action inhibitor 1-MCP efficiently blocked fruit maturation, even following SlTOR inhibition. These results suggest that accelerated fruit ripening caused by SlTOR inhibition depends on ethylene, and that SlTOR may function as a regulator in ethylene metabolism.