Abstract

Premature petal senescence dramatically reduces flower quality and value. Ethylene and reactive oxygen species (ROS) are key players in accelerating rose petal senescence, but the molecular mechanism by which ethylene antagonizes ROS scavenging is not well understood. Here, we show that ethylene reduces ascorbic acid (AsA) production, leading to the accumulation of ROS and hastening petal senescence. Ethylene treatment suppresses the expression of GDP-L-galactose phosphorylase 1 (RhGGP1), encoding the rate-controlling enzyme in AsA biosynthesis. A HOMEODOMAIN-LEUCINE ZIPPER (HD-ZIP) II transcriptional factor, RhHB22, directly binds to the promoter of RhGGP1 and inhibits its transcription. RhHB22 is induced by ethylene, and silencing of RhHB22 increases RhGGP1 expression and AsA production, resulting in reduced H2O2 accumulation and delayed petal senescence. Additionally, the delayed petal senescence symptoms of RhHB22-silenced plants were suppressed by silencing RhGGP1. Moreover, the expression of RhGGP1, which is suppressed by ethylene in wild-type petals, is significantly compromised in RhHB22-silenced petals. These findings uncover the transcriptional regulatory mechanism by which ethylene promotes ROS accumulation and petal senescence by inhibiting AsA biosynthesis, enhance our understanding of ethylene-induced petal senescence, and provide novel insights for improving the longevity of cut flowers.

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