Sweet grapes do not happen by accident. As berries ripen, the plant has to move, make, and store sugars with remarkable timing, and even small shifts can affect flavor, harvest quality, and market value.
A new study in Horticulture Research traces part of that process to a specific molecular chain in grapes, showing how the ripening hormone abscisic acid, or ABA, helps drive sugar buildup. Researchers at Shanghai Jiao Tong University found that ABA sped ripening in ‘Muscat Hamburg’ grapes and increased soluble sugar accumulation, then linked that change to two transcription factors, VvMYB44 and VvERF045, and a sucrose-related gene called VvSPS4.
The findings gives grape biology a more defined route between hormone signaling and sweetness. Rather than treating ABA as a broad ripening signal with many downstream effects, the study identifies a narrower control point tied to sucrose metabolism.
That matters because sweetness is one of the traits people notice first.
The team treated pre-veraison grape berries with 500 mg L−1 ABA and tracked changes over four stages of development. The treated fruit colored earlier, expanded more, and built up total soluble solids faster than untreated berries. Glucose and fructose also rose more quickly and reached higher levels under ABA treatment, while sucrose stayed low and did not show a significant change at 36 days after treatment.
Those changes fit with what growers and plant scientists have long associated with ABA. In fleshy fruits, especially non-climacteric fruits such as grapes, the hormone has been tied to ripening traits including color, flavor, and sugar content. What has been less clear is how that signal reaches the machinery that handles sugars inside the berry.
To dig into that question, the researchers sequenced RNA from 21 grape samples and looked for genes that moved in step with rising sugar levels. Across those samples, 26,087 genes were expressed. Clean reads ranged from 5.92 to 10.24 Gb per sample, with Q30 values of at least 91.99%, and mapping rates from 68.48% to 92.76%.
They then used weighted gene co-expression network analysis to sort genes into groups linked to traits such as fructose, glucose, and sucrose accumulation during ripening.
From that network, the team identified 19 structural genes involved in sugar metabolism and transport, plus 135 transcription factors. After narrowing the list, they focused on 12 structural genes strongly tied to sugar accumulation and 128 transcription factors correlated with them. Among those candidates, five structural genes and 44 transcription factors differed between ABA-treated and control fruit.
One of those regulators, VvMYB44, drew special attention because it showed the highest expression in mature ABA-treated fruit among the 44 transcription factors highlighted by the analysis.
VvMYB44 belongs to the R2R3-MYB family and sits in the nucleus, where transcription factors usually do their work. In grape berries, its transcript abundance stayed high from 60 to 110 days post anthesis, a span that covers development and ripening.
The team then tested what happened when they pushed the gene harder. In grape calli overexpressing VvMYB44, glucose, fructose, and sucrose all rose significantly compared with wild type. Tomato lines engineered to overexpress the grape gene also produced fruit with significantly higher soluble sugar contents.
That cross-species result does not prove the same pathway runs identically in every fruit crop, but it did strengthen the case that VvMYB44 acts as a positive regulator of sugar accumulation.
The next step was figuring out what VvMYB44 actually targets.
The researchers examined candidate genes in the sugar network and found that VvMYB44 was strongly correlated with 10 structural genes tied to sugar metabolism, including invertases, sucrose synthases, SPS genes, and a sugar transporter. They narrowed the likely direct targets further, and one promoter stood out: VvSPS4 contained a binding motif for AtMYB44.
Several experiments backed that up. A yeast one-hybrid assay showed that VvMYB44 bound the VvSPS4 promoter. An electrophoretic mobility shift assay confirmed direct binding to the MBS motif, and mutated probes disrupted that binding. A dual-luciferase assay in tobacco leaves then showed that VvMYB44 activated the VvSPS4 promoter.
Put simply, VvMYB44 appears to switch on VvSPS4.
That is an important finding because SPS enzymes sit at a key step in sucrose synthesis. The paper describes SPS as the rate-limiting enzyme in that pathway, and other fruit studies have also connected SPS activity with rising sucrose content during ripening.
The story did not stop with one transcription factor.
The researchers found that VvERF045 physically interacts with VvMYB44. They showed that connection with yeast two-hybrid, pull-down, bimolecular fluorescence complementation, and co-immunoprecipitation assays. In both in vitro and in vivo tests, the proteins behaved like partners.
When both were present, the activation of VvSPS4 got stronger. Dual-luciferase assays in tobacco leaves showed that co-expression of VvMYB44 and VvERF045 increased VvSPS4-driven luminescence beyond what VvMYB44 could do alone.
Tomato lines overexpressing VvERF045 also accumulated significantly higher levels of glucose, fructose, and sucrose than wild type fruit.
Together, the results point to a cooperative module: ABA promotes ripening and sugar accumulation, VvMYB44 activates VvSPS4, and VvERF045 strengthens that activation through protein interaction.
The work adds a sharper mechanism to a field that often has to infer function from hormone treatments and large gene-expression datasets. The authors note that fruit-ripening research has long been limited by the lack of extensive mutant collections in fruit crops, so many studies rely on hormone applications followed by transcriptomic or metabolomic analysis.
This study follows that pattern, then goes further with binding assays and overexpression experiments in grape calli and tomato. Even so, its evidence comes from exogenous ABA treatment, expression networks, and transgenic overexpression systems rather than from mutant collections in grape berries themselves.
That does not weaken the finding that the VvMYB44-VvERF045-VvSPS4 module is a strong candidate pathway. It does mean the work sits within the practical limits the paper itself describes for fruit-ripening research.
For grape breeding and crop improvement, the study highlights a possible molecular target for sweetness. Instead of treating sugar buildup as a diffuse outcome of ripening, breeders and plant biologists now have a more specific regulatory chain to examine.
The pathway could also help future efforts to manage harvest quality and ripening traits in grapes. Because VvMYB44 and VvERF045 both increased sugar accumulation in experimental systems, the module may offer a route for improving flavor-related traits in grapes and possibly other horticultural crops.
More broadly, the work helps connect hormone signaling with the genes that shape fruit quality, a link with clear value in both basic plant biology and premium fruit production.
Research findings are available online in the journal Horticulture Research.
The original story “Scientists discover the genetic cause of sweeter grapes” is published in The Brighter Side of News.
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