Abstract

This article focuses on the molecular and hormonal mechanisms underlying the control of fleshy fruit ripening and quality. Recent research on tomato shows that ethylene, acting through transcription factors, is responsible for the initiation of tomato ripening. Several other hormones, including abscisic acid (ABA), jasmonic acid (JA) and brassinosteroids (BR), promote ripening by upregulating ethylene biosynthesis genes in different fruits. Changes to histone marks and DNA methylation are associated with the activation of ripening genes and are necessary for ripening initiation. Light, detected by different photoreceptors and operating through ELONGATED HYPOCOTYL 5(HY5), also modulates ripening. Re-evaluation of the roles of ‘master regulators’ indicates that MADS-RIN, NAC-NOR, Nor-like1 and other MADS and NAC genes, together with ethylene, promote the full expression of genes required for further ethylene synthesis and change in colour, flavour, texture and progression of ripening. Several different types of non-coding RNAs are involved in regulating expression of ripening genes, but further clarification of their diverse mechanisms of action is required. We discuss a model that integrates the main hormonal and genetic regulatory interactions governing the ripening of tomato fruit and consider variations in ripening regulatory circuits that operate in other fruits.

Highlights

  • Fruits can develop from several different parts of a flower and possess different characteristics

  • There are many reports showing that auxin, abscisic acid (ABA) and jasmonic acid (JA) influence expression of genes involved in the biosynthesis of ethylene and other aspects of the ripening control network, as discussed later

  • SlARF2A is ethylene-regulated, while SlARF2B is auxin-induced [141]. These results indicate substantial interactions between ethylene and auxin in the regulation of auxin response factors (ARFs) and ethylene response factor TFs (ERFs)

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Summary

Introduction

Fruits can develop from several different parts of a flower and possess different characteristics. Non-climacteric fruits do not, show a burst of CO2 or ethylene production, which is the classic sign of ripening onset in climacteric fruit This distinction between two types of fruits is somewhat arbitrary, and ripening of both types of fruits involves hormones and similar changes in gene expression, often regulated by structurally related transcription factors (TFs). Tomato has been an important ripening model [3,8,9,10,11,12], the fact that ripening has arisen several times during the course of evolution, and the differences between climacteric and non-climacteric fruits, caution against a “one type fits all” model [13]. We consider important information garnered from research on a range of fruits, where this has enhanced our understanding of ripening, and develop a model of how the different aspects of the ripening processes are integrated

Main Physiological and Biochemical Changes Are Regulated by Ripening Genes
Colour Changes during Ripening
Fruit Softening
Ripening Is Influenced by Multiple Hormones and Light
Ethylene Initiates and Promotes Ripening
Auxin Delays Ripening and Antagonises the Effects of Ethylene
Jasmonates
Brassinosteroids
Influence of Light of Different Wavelengths on Ripening
DNA Methylation
Histone Marks
Non-Coding RNAs
The Identification and Function of Major Regulator TFs
The Wider Importance of the NAC Gene Family
Conclusions and Models for the Control of Ripening
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