Abstract

Fruit set is the earliest phase of fruit growth and represents the onset of ovary growth after successful fertilization. In parthenocarpy, fruit formation is less affected by environmental factors because it occurs in the absence of pollination and fertilization, making parthenocarpy a highly desired agronomic trait. Elucidating the genetic program controlling parthenocarpy, and more generally fruit set, may have important implications in agriculture, considering the need for crops to be adaptable to climate changes. Several phytohormones play an important role in the transition from flower to fruit. Further complexity emerges from functional analysis of floral homeotic genes. Some homeotic MADS-box genes are implicated in fruit growth and development, displaying an expression pattern commonly observed for ovary growth repressors. Here, we provide an overview of recent discoveries on the molecular regulatory gene network underlying fruit set in tomato, the model organism for fleshy fruit development due to the many genetic and genomic resources available. We describe how the genetic modification of components of this network can cause parthenocarpy, discussing the contribution of hormonal signals and MADS-box transcription factors.

Highlights

  • The Transition from Flower to Fruit in TomatoTomato is one of the most important crops worldwide cultivated for the nutritional value of its fruit, which is a source of health-promoting compounds such as vitamins, carotenoids, phenolic compounds, and small peptides [1]

  • These studies revealed that parthenocarpy can be achieved by manipulating auxin action at different levels, by acting on its biosynthesis, signaling cascade, and transport, corroborating the crucial role played by this hormone in the control of fruit set

  • It has been suggested that the role of abscisic acid (ABA) during fruit set is to inhibit the growth of the ovary maintaining the pistil in its dormant state, acting as the antagonist of the promoting roles played by IAA and GAs [65,74]

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Summary

Introduction

Tomato is one of the most important crops worldwide cultivated for the nutritional value of its fruit, which is a source of health-promoting compounds such as vitamins, carotenoids, phenolic compounds, and small peptides [1]. Studies conducted principally on model species, such as Arabidopsis thaliana and Antirrhinum majus, revealed that from flower initiation to the development of the mature flower (anthesis), the floral organs develop in concert, through a tightly controlled genetic regulation where the MADS-box transcription factor family plays a significant role [3]. Fruit growth continues through cell expansion (phase III) until ripening, which in tomato normally occurs ~35 days after fruit set [10]. We review the recent discoveries on the molecular regulatory gene network underlying fruit set, and we describe how genetic modification of components of this network can cause parthenocarpy, with particular reference to the contribution of hormonal signals and MADS-box transcription factors

Auxins
Other Hormones
Parthenocarpy and MADS-box Transcription Factors
Concluding Remarks
Full Text
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