# Unravelling the Molecular Regulation Mechanisms of Slow Ripening Trait in _Prunus persica_
## 1 Introduction  
Fruit development is a complex process that involves the interplay of cell division, expansion, and the differentiation of plant tissues, and it is carefully coordinated by many metabolic pathways controlling numerous traits such as color, aroma, size, and flavor [1, 2]. Moreover, in parallel with the normal ripening (NR) process, many physiological changes occur in fruit, such as softening, fruit growth, seed development, sugar accumulation and acidity reduction, background and color skin changes, synthesis of volatile compounds, among others [2, 3]. In peach, fruit ripening is characterized by presenting a double sigmoid fruit growth curve in which four stages named S1, S2, S3, and S4 can be identified. The S1 period is the first fruit growth step characterized by cell division followed by cell expansion. In S2, the fruit growth decreased significantly, and the endocarp lignification process began. Then, the second fruit growth step occurred in S3 by cell expansion, and fruit maturation was complete at the end of this period. Finally, ripening is the period corresponding to S4 [4]. Several plant hormones play an essential role in this complex maturity process temporarily and spatially synchronizing the different fruit developmental stages [1]. Auxins, gibberellins (GA), cytokins, ethylene, jasmonic acid (JA), and abscisic acid (ABA) havebeen identified to be involved in different fruit stages controlling the normal fruit growth [5]. It was reported that auxins, GA, and in some cases cytokins play crucial roles in fruits [6]. For instance, it was suggested that an auxin-mediated promotion of GA synthesis occurs after fertilization in the ovules and valves, thereby stimulating fruit growth [7]. While auxins are described by initiating fruit development and, with gibberells maintaining fruit growth, ethylene is the senescence hormone. Ethylene evolution during fruit maturation in peach was described by [8]. This hormone was observed during the early S1 stage and in ripening (the end of S4), with the highest concentration values during ripening being positively associated with high activity levels of the enzyme 1-aminocyclopropane-1-carboxylic acid oxidase (ACO). Jasmonic acid (JA) mediates plant responses to environmental stresses such as wounding, insects, and pathogen attack [9], but it also plays a role during developmental processes, including root growth, seed germination, pollen and fruit development, and ripening [10]. On the other hand, the hormone abscisic acid (ABA) was related with the stimulation of color development and sugar accumulation during fruit ripening in peach, and associated with the modulation of the biosynthesis of ethylene and auxins by strongly affecting related gene expression during the S3/S4 developmental stages [11]. As previously mentioned, peach fruit ripening is accompanied by changes in color, aroma, size, and flavor. These changes are controlled by complex hormonal machinery allowing to development of a normal ripen fruit. For the first time, a nectarine genotype originated from Fantasia incapable of ripening and described as the slow ripening (SR) phenotype was identified [12]. Slow ripening fruit remained firm and green and exhibited no rise in CO\({}_{2}\) or ethylene production rates during more than one month at 20 \({}^{\circ}\)C. Previous studies have suggested that this trait is controlled by a single recessive gene (sr) [13], and by comparing the seed and mesocarp development between the Fantasia and SR phenotypes, it was evident that the mesocarp development of SR individuals seems to be blocked at stage S3 [4]. Furthermore, a deletion of 26.6 kbp was identified in an F2 population from the self-pollination of Venus (V \(\times\) V) associated with this trait [14], and a diagnostic marker was developed for the SR phenotype in a Belbiente and Nectalady (Bb \(\times\) Nl) population [15].