Litchi Fruit LcNAC1 is a Target of LcMYC2 and Regulator of Fruit Senescence Through its Interaction with LcWRKY1.

Senescence is a key factor resulting in deterioration of non-climacteric fruit. NAC transcription factors are important regulators in plant development and abiotic stress responses, yet little information regarding the role of NACs in regulating non-climacteric fruit senescence is available. In this study, we cloned 13 NAC genes from litchi (Litchi chinensis) fruit, and analyzed subcellular localization and expression profiles of these genes during post-harvest natural and low-temperature-delayed senescence. Of the 13 NAC genes, expression of LcNAC1 was up-regulated in the pericarp and pulp as senescence progressed, and was significantly higher in senescence-delayed fruit than that in naturally senescent fruit. LcNAC1 was induced by exogenous ABA and hydrogen peroxide. Yeast one-hybrid analysis and transient dual-luciferase reporter assay showed that LcNAC1 was positively regulated by the LcMYC2 transcription factor. LcNAC1 activated the expression of LcAOX1a, a gene associated with reactive oxygen species regulation and energy metabolism, whereas LcWRKY1 repressed LcAOX1a expression. In addition, LcNAC1 interacted with LcWRKY1 in vitro and in vivo. These results indicated that LcNAC1 and LcWRKY1 form a complex to regulate the expression of LcAOX1a antagonistically. Taken together, the results reveal a hierarchical and co-ordinated regulatory network in senescence of harvested litchi fruit.