A sweet cherry AGAMOUS-LIKE transcription factor PavAGL15 affects fruit size by directly repressing the PavCYP78A9 expression

Abstract

Fruit size, as an important fruit quality trait, is strongly associated with the commercial value of sweet cherry (Prunus avium L.). Understanding the genetic mechanisms underlying the control of fruit size is essential for breeding new varieties with larger fruit to increase yield and economic value. However, little is known about the molecular mechanisms underlying fruit size in sweet cherry. Here, we identified and functionally characterized a MIKC-type MADS-box transcription factor, PavAGL15, in sweet cherry, as a putative protein that binds the promoter of PavCYP78A9, a cytochrome P450, which controls sweet cherry fruit size. Yeast one-hybrid and transient dual-luciferase reporter assays indicated that PavAGL15 directly bound to the PavCYP78A9 promoter in vitro and in vivo, resulting in repressing expression. PavAGL15 was expressed at high levels in flower buds, blossoms and young fruit as assessed by real-time PCR. The PavAGL15 protein localized to the nucleus. Silencing PavAGL15 using virus-induced gene silencing significantly increased the fruit size, which caused the high expression levels of PavCYP78A9, cell cycling and proliferation-related genes in sweet cherry fruits. Collectively, these results demonstrate that PavAGL15 is a negative regulator of sweet cherry fruit size that regulates PavCYP78A9 expression at the transcriptional level. Thus, we have gained new insights into the regulatory networks affecting fruit size during sweet cherry fruit growth and development.