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Auxin Treatment Enhances Anthocyanin Production in the Non-Climacteric Sweet Cherry (Prunus avium L.).

ABSTRACT: Abscisic acid (ABA) is a key signaling molecule promoting ripening of non-climacteric fruits such as sweet cherry (Prunus avium L.). To shed light on the role of other hormones on fruit development, ripening and anthocyanin production, the synthetic auxin 1-naphthaleneacetic acid (NAA) was applied to sweet cherry trees during the straw-color stage of fruit development. NAA-treated fruits exhibited higher concentrations of 1-aminocyclopropane-1-carboxylic acid (ACC) and ABA-glucose ester (ABA-GE), which are a precursor of ethylene and a primary storage form of ABA, respectively. Consistent with these observations, transcript levels of genes encoding ACC synthase and ACC oxidase, both involved in ethylene biosynthesis, were increased after 6 days of NAA treatment, and both ABA concentration and expression of the regulator gene of ABA biosynthesis (NCED1 encoding 9-cis-epoxycarotenoid dioxygenase) were highest during early fruit ripening. In addition, transcript levels of key anthocyanin regulatory, biosynthetic and transport genes were significantly upregulated upon fruit exposure to NAA. This was accompanied by an increased anthocyanin concentration and fruit weight whilst fruit firmness and cracking index decreased. Altogether our data suggest that NAA treatment alters ethylene production, which in turn induces ripening in sweet cherry and enhanced anthocyanin production, possibly through ABA metabolism. The results from our study highlight the potential to use a single NAA treatment for manipulation of cherry ripening.

SUBMITTER: Clayton-Cuch D

PROVIDER: S-EPMC8509301 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:The harvesting of sweet cherry (Prunus avium L.) fruit is a labor-intensive process. The mechanical harvesting of sweet cherry fruit is feasible; however, it is dependent on the formation of an abscission zone at the fruit-pedicel junction. The natural propensity for pedicel-fruit abscission zone (PFAZ) activation varies by cultivar, and the general molecular basis for PFAZ activation is not well characterized. In this study, ethylene-inducible change in pedicel fruit retention force (PFRF) was recorded in a developmental time-course with a concomitant analysis of the PFAZ transcriptome from three sweet cherry cultivars. In 'Skeena', mean PFRF for both control and treatment fruit dropped below the 0.40 kg-force (3.92 N) threshold for mechanical harvesting, indicating the activation of a discrete PFAZ. In 'Bing', mean PFRF for both control and treatment groups decreased over time. However, a mean PFRF conducive to mechanical harvesting was achieved only in the ethylene-treated fruit. While in 'Chelan' the mean PFRF of the control and treatment groups did not meet the threshold required for efficient mechanical harvesting. Transcriptome analysis of the PFAZ region followed by the functional annotation, differential expression analysis, and gene ontology (GO) enrichment analyses of the data facilitated the identification of phytohormone-responsive and abscission-related transcripts, as well as processes that exhibited differential expression and enrichment in a cultivar-dependent manner over the developmental time-course. Additionally, read alignment-based variant calling revealed several short variants in differentially expressed genes, associated with enriched gene ontologies and associated metabolic processes, lending potential insight into the genetic basis for different abscission responses between the cultivars. These results provide genetic targets for the induction or inhibition of PFAZ activation, depending on the desire to harvest the fruit with or without the stem attached. Understanding the genetic mechanisms underlying the development of the PFAZ will inform future cultivar development while laying a foundation for mechanized sweet cherry harvest.

Project description:BackgroundFruit color is one of the most important economic traits of the sweet cherry (Prunus avium L.). The red coloration of sweet cherry fruit is mainly attributed to anthocyanins. However, limited information is available regarding the molecular mechanisms underlying anthocyanin biosynthesis and its regulation in sweet cherry.Methodology/principal findingsIn this study, a reference transcriptome of P. avium L. was sequenced and annotated to identify the transcriptional determinants of fruit color. Normalized cDNA libraries from red and yellow fruits were sequenced using the next-generation Illumina/Solexa sequencing platform and de novo assembly. Over 66 million high-quality reads were assembled into 43,128 unigenes using a combined assembly strategy. Then a total of 22,452 unigenes were compared to public databases using homology searches, and 20,095 of these unigenes were annotated in the Nr protein database. Furthermore, transcriptome differences between the four stages of fruit ripening were analyzed using Illumina digital gene expression (DGE) profiling. Biological pathway analysis revealed that 72 unigenes were involved in anthocyanin biosynthesis. The expression patterns of unigenes encoding phenylalanine ammonia-lyase (PAL), 4-coumarate-CoA ligase (4CL), chalcone synthase (CHS), chalcone isomerase (CHI), flavanone 3-hydroxylase (F3H), flavanone 3'-hydroxylase (F3'H), dihydroflavonol 4-reductase (DFR), anthocyanidin synthase (ANS) and UDP glucose: flavonol 3-O-glucosyltransferase (UFGT) during fruit ripening differed between red and yellow fruit. In addition, we identified some transcription factor families (such as MYB, bHLH and WD40) that may control anthocyanin biosynthesis. We confirmed the altered expression levels of eighteen unigenes that encode anthocyanin biosynthetic enzymes and transcription factors using quantitative real-time PCR (qRT-PCR).Conclusions/significanceThe obtained sweet cherry transcriptome and DGE profiling data provide comprehensive gene expression information that lends insights into the molecular mechanisms underlying anthocyanin biosynthesis. These results will provide a platform for further functional genomic research on this fruit crop.

Project description:BACKGROUND AND AIMS: The cuticular membrane (CM) of Prunus avium (sweet cherry) and other fleshy fruit is under stress. Previous research indicates that the resultant strain promotes microscopic cuticular cracking. Microcracks impair the function of the CM as a barrier against pathogens and uncontrolled water loss/uptake. Stress and strain result from a cessation of CM deposition during early development, while the fruit surface continues to expand. The cessation of CM deposition, in turn, may be related to an early downregulation of CM-related genes. The aims of this study were to identify genes potentially involved in CM formation in sweet cherry fruit and to quantify their expression levels. METHODS: Fruit growth and CM deposition were quantified weekly from anthesis to maturity and rates of CM deposition were calculated. Sequences of genes expressed in the sweet cherry fruit skin (exocarp) were generated using high-throughput sequencing of cDNA and de novo assembly and analysed using bioinformatics tools. Relative mRNA levels of selected genes were quantified in the exocarp and fruit flesh (mesocarp) weekly using reverse transcriptase-quantitative real-time PCR and compared with the calculated CM deposition rate over time. KEY RESULTS: The rate of CM deposition peaked at 93 (±5) ?g per fruit d(-1) about 19 d after anthesis. Based on sequence analyses, 18 genes were selected as potentially involved in CM formation. Selected sweet cherry genes shared up to 100 and 98 % similarity with the respective Prunus persica (peach) and Arabidopsis thaliana genes. Expression of 13 putative CM-related genes was restricted to the exocarp and correlated positively with the CM deposition rate. CONCLUSIONS: The results support the view that the cessation of CM deposition during early sweet cherry fruit development is accounted for by a downregulation of genes involved in CM deposition. Genes that merit further investigation include PaWINA, PaWINB, PaLipase, PaLTPG1, PaATT1, PaLCR, PaGPAT4/8, PaLACS2, PaLACS1 and PaCER1.

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Auxin Treatment Enhances Anthocyanin Production in the Non-Climacteric Sweet Cherry (Prunus avium L.).

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