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Kiwifruit (Actinidia spp.) is a recently domesticated fruit crop with several novel‐coloured cultivars being developed. Achieving uniform fruit flesh pigmentation in red genotypes is challenging. To investigate the cause of colour variation between fruits, we focused on a red‐fleshed Actinidia chinensis var. chinensis genotype. It was hypothesized that carbohydrate supply could be responsible for this variation. Early in fruit development, we imposed high or low (carbon starvation) carbohydrate supplies treatments; carbohydrate import or redistribution was controlled by applying a girdle at the shoot base. Carbon starvation affected fruit development as well as anthocyanin and carbohydrate metabolite concentrations, including the signalling molecule trehalose 6‐phosphate. RNA‐Seq analysis showed down‐regulation of both gene‐encoding enzymes in the anthocyanin and carbohydrate biosynthetic pathways. The catalytic trehalose 6‐phosphate synthase gene TPS1.1a was down‐regulated, whereas putative regulatory TPS7 and TPS11 were strongly up‐regulated. Unexpectedly, under carbon starvation MYB10, the anthocyanin pathway regulatory activator was slightly up‐regulated, whereas MYB27 was also up‐regulated and acts as a repressor. To link these two metabolic pathways, we propose a model where trehalose 6‐phosphate and the active repressor MYB27 are involved in sensing the carbon starvation status. This signals the plant to save resources and reduce the production of anthocyanin in fruits. In carbon‐starved red‐fleshed kiwifruit, both carbohydrate and anthocyanin concentrations were greatly reduced. Our model suggests that anthocyanin biosynthesis was actively repressed by MYB27 via trehalose 6‐phosphate signalling to conserve carbon. [ABSTRACT FROM AUTHOR]

In fleshy fruit species that have a strong requirement for ethylene to ripen, ethylene is synthesized autocatalytically, producing increasing concentrations as the fruits ripen. Apple fruit with the ACC OXIDASE 1 (ACO1) gene suppressed cannot produce ethylene autocatalytically at ripening. Using these apple lines, an ethylene sensitivity dependency model was previously proposed, with traits such as softening showing a high dependency for ethylene as well as low sensitivity. In this study, it is shown that the molecular control of fruit softening is a complex process, with different cell wall-related genes being independently regulated and exhibiting differential sensitivities to and dependencies on ethylene at the transcriptional level. This regulation is controlled through a dose × time mechanism, which results in a temporal transcriptional response that would allow for progressive cell wall disassembly and thus softening. This research builds on the sensitivity dependency model and shows that ethylene-dependent traits can progress over time to the same degree with lower levels of ethylene. This suggests that a developmental clock measuring cumulative ethylene controls the fruit ripening process.