MaC2H2-like regulates chilling stress response of 'Fenjiao' banana by modulating flavonoid synthesis and fatty acid desaturation.

Abstract

Chilling injury (CI) is a major problem that affects fruit quality and ripening. Herein, chilling stress severely inhibited the expression of transcription factor MaC2H2-like. MaC2H2-like activates the expression of genes associated with flavonoid synthesis (MaC4H-like1, Ma4CL-like1, MaFLS, and MaFLS3) and fatty acid desaturation (MaFAD6-2 and MaFAD6-3), the leading indicators of chilling tolerance. MaC2H2-like interacts with MaEBF1 and boosts the transcriptional activity of MaFAD6-2, MaFAD6-3, Ma4CL-like1, and MaFLS. The overexpression of MaC2H2-like reduced fruit CI, induced the expression of these genes and increased the content of flavonoid and unsaturated fatty acid. Meanwhile, the silencing of MaC2H2-like increased fruit CI and downregulated the expression of those genes and reduced the content of flavonoid and unsaturated fatty acid. These results indicate that MaC2H2-like function as new player in modulating fruit CI by regulating flavonoid synthesis and fatty acid desaturation. MaC2H2-like could be a useful candidate gene for improving cold tolerance in 'Fenjiao' banana.