Genetic analysis of a white-to-red berry skin color reversion and its transcriptomic and metabolic consequences in grapevine (Vitis vinifera cv. 'Moscatel Galego').

BACKGROUND: Somatic mutations occurring within meristems of vegetative propagation material have had a major role in increasing the genetic diversity of the domesticated grapevine (Vitis vinifera subsp. vinifera). The most well studied somatic variation in this species is the one affecting fruit pigmentation, leading to a plethora of different berry skin colors. Color depletion and reversion are often observed in the field. In this study we analyzed the origin of a novel white-to-red skin color reversion and studied its possible metabolic and transcriptomic consequences on cv. 'Muscat à Petits Grains Blancs' (synonym cv. 'Moscatel Galego Branco'), a member of the large family of Muscats. RESULTS: The mild red-skinned variant (cv. 'Muscat à Petits Grains Rouge', synonym cv. 'Moscatel Galego Roxo'), characterized by a preferential accumulation of di-hydroxylated anthocyanins, showed in heterozygosis a partially-excised Gret1 retrotransposon in the promoter region of the MYBA1 anthocyanin regulator, while MYBA2 was still in homozygosis for its non-functional allele. Through metabolic (anthocyanin, resveratrol and piceid quantifications) and transcriptomic (RNA-Seq) analyses, we show that within a near-isogenic background, the transcriptomic consequences of color reversion are largely associated to diminished light/UV-B responses probably as a consequence of the augment of metabolic sunscreens (i.e. anthocyanins). CONCLUSIONS: We propose that the reduced activity of the flavonoid tri-hydroxylated sub-branch and decreased anthocyanin synthesis and modification (e.g. methylation and acylation) are the potential causes for the mild red-skinned coloration in the pigmented revertant. The observed positive relation between anthocyanins and stilbenes could be attributable to an increased influx of phenylpropanoid intermediaries due to the replenished activity of MYBA1, an effect yet to be demonstrated in other somatic variants.