Hormone metabolism regulates fruit maturation in a slow ripening grape genotype

Abstract

Context and purpose of the study. Rising temperatures and prolonged heat accelerate berry sugar accumulation in advance of the accumulation of compounds responsible for aroma, colour and mouthfeel. This uncoupling of sugar accumulation from key berry quality constituents often reduces fruit and wine quality. Identification of genetic material with reduced rates of sugar accumulation when grown under warm conditions offers a potential solution. Previous work in our laboratory found that the maturation rate of a grape selection with abnormally slow ripening could be restored with hormone treatments, suggesting that the slow ripening phenotype may be regulated by hormone metabolism. This study aims to identify the candidate genes driving this phenotype by performing a deep transcriptomic analysis and characterizing hormone dynamics.

Material and methods. Over three years, samples were collected weekly for soluble solids, berry weight and firmness in a white-fruited grape selection displaying slow ripening and a full sibling of the selection with normal ripening. The slow ripening selection fruit was treated with 2000 ppm abscisic acid (S-ABA, ProTone, Valent Biosciences) using Tween20 (0.1% v/v) as surfactant. Hormone analyses were conducted on samples at pre-, mid-, and post-veraison stages for both genotypes and ABA-treated and untreated fruit for the slow ripening genotype. Gene expression analysis was performed using RNA-seq on the same samples.

Results. The onset of berry softening in the slow ripening selection was delayed 45 days compared to its normal ripening sibling. Reduced levels of free ABA and higher inactive auxin conjugation were observed in the slow ripening selection, suggesting a blockage of signals in the early ripening phase. ABA treatment accelerated the maturation of the slow ripening selection, and its free ABA levels were similar to those of the normal ripening selection. Differentially expressed genes (DEGs) associated with hormone metabolism, transcription factors, and other ripening-related processes were found when comparing slow vs normal ripening and ABA-treated vs untreated fruit. The data suggested an active disruption of metabolic pathways regulating auxins and ABA cross-signaling, essential to orchestrating the onset of berry maturation in the slow ripening selection. Further studies are needed to identify the genomic regions responsible for the slow ripening trait and evaluate this genotype’s use for cultivar improvement.