Sugar content is related to fruit sweetness, and the complex mechanisms underlying fruit sugar accumulation still remain elusive. Here, we report a peach PpTST1 gene encoding tonoplast sugar transporter that is located in the quantitative trait loci (QTL) interval on Chr5 controlling fruit sucrose content. One derived Cleaved Amplified Polymorphic Sequence (dCAPS) marker was developed based on a nonsynonymous G/T variant in the third exon of PpTST1. Genotyping of peach cultivars with the dCAPS marker revealed a significant difference in fruit sugar content among genotypes. PpTST1 is located in the tonoplast, and substitution of glutamine by histidine caused by the G/T variation has no impact on subcellular location. The expression profile of PpTST1 exhibited a consistency with the sugar accumulation pattern, and its transient silencing significantly inhibited sugar accumulation in peach fruits. All of these results demonstrated the role of PpTST1 in regulating sugar accumulation in peach fruit. In addition, cis-elements for binding of MYB and WRKY transcript factors were found in the promoter sequence of PpTST1,suggesting a gene regulatory network of fruit sugar accumulation. Our results are not only helpful for understanding the mechanisms underlying fruit sugar accumulation, but will also be useful for the genetic improvement of fruit sweetness in peach breeding programs.
Peach (Prunus persica) is a climacteric fruit with a relatively short shelf life due to its fast ripening or softening process. Here, we report the association of gene families encoding ethylene insensitive-3 like (EIL) and ethylene response factor (ERF) with fruit ripening in peach. In total, 3 PpEILs and 12 PpERFs were highly expressed in fruit, with the majority showing a peak of expression at different stages. All three EILs could activate ethylene biosynthesis genes PpACS1 and PpACO1. One out of the 12 PpERFs, termed PpERF.E2, is a homolog of ripening-associated ERFs in tomato, with a consistently high expression throughout fruit development and an ability to activate PpACS1 and PpACO1. Additionally, four subgroup F PpERFs harboring the EAR repressive motif were able to repress the PpACO1 promoter but could also activate the PpACS1 promoter. Promoter deletion assay revealed that PpEILs and PpERFs could participate in transcriptional regulation of PpACS1 through either direct or indirect interaction with various cis-elements. Taken together, these results suggested that all three PpEILs and PpERF.E2 are candidates involved in ethylene biosynthesis, and EAR motif-containing PpERFs may function as activator or repressor of ethylene biosynthesis genes in peach. Our study provides an insight into the roles of EILs and ERFs in the fruit ripening process.
Purple acid phosphatases (PAPs) play a key role in phosphorus (P) assimilation and redistribution in plants, catalyzing the hydrolysis of phosphate esters to produce inorganic phosphate (Pi). In this study, a total of 77 PAP genes were identified in B. napus. The candidate genes were divided into three groups and ten subgroups based on the phylogenetic analyses and exon-intron organization. Among these 77 BnaPAP proteins, 35 exhibit typical metal-ligating residues characteristic of known PAPs, whereas certain unaltered amino acid residues were absent or displaced in other BnaPAPs. A computational prediction was conducted, revealing that the majority of PAPs contain signal peptide motifs and display a range of N-glycosylation levels, as well as transmembrane helix motifs. An analysis of previously obtained RNA-seq data revealed that 55.84% (43 of 77) of the BnaPAPs responded to Pi deficiency. Moreover, we conducted a preliminary examination of the expression profiles of BnaPAP genes in response to salt stress, and discovered that 42.86% (33 of 77) of these genes were induced under salt stress, either in the shoots or in the roots. Further qRT-PCR and GUS analyses revealed that BnaC9.PAP10 and BnaA7.PAP10, two paralogs of BnaPAP10s, were induced by Pi deficiency. Notably, BnaC9.PAP10 exhibits robust induction, compared to the relatively mild induction observed in BnaA7.PAP10. Our research shows that BnaA7.PAP10 uniquely responds to Pi stress via the W-box, while BnaA7.PAP10 predominantly responds via the P1BS element, and the differences in cis-regulatory elements (CREs) within their promoter regions specifically contribute to their distinct expression levels under Pi stress. Our findings provide valuable insights and establish a foundation for future functional studies of BnaPAPs.