Abstract

BackgroundBlossom-end rot in tomatoes is often used as a model system to study fruit calcium deficiency. The study of blossom-end rot development in tomatoes has been greatly impeded by the difficulty of directly studying and applying treatments to the affected cells. This manuscript presents a novel method for studying blossom-end rot development after harvest in immature whole fruit and in pericarp discs.ResultsPericarp discs removed from the bottom pericarp of immature healthy fruit developed blossom-end rot like symptoms, corresponding to a decrease in L* value and an increase in a* value. Symptoms also developed in columella tissue, but not in stem-end pericarp tissue, similar to patterns observed during blossom-end rot development on the plant. Ascorbate oxidase and peroxidase activity, which are elevated in blossom-end rot affected fruit compared to healthy fruit, were both correlated with colorimetric measures of tissue darkening in discs. Respiration rate was higher in discs that later developed blossom-end rot symptoms, with increased respiration in asymptomatic discs on day 1 of storage being associated with symptom development on day 2. Calcium chloride and ascorbic acid treatments inhibited symptom development, demonstrating the potential of this method to provide causal evidence.ConclusionsResults indicate that symptom development in this system is consistent with blossom-end rot development with regards to location, color change, and the activity of key enzymes. This system has the potential to be used to elucidate the cause of fruit calcium deficiency and improve knowledge of the biological basis for calcium’s diverse effects on fruit.

Highlights

  • Blossom-end rot in tomatoes is often used as a model system to study fruit calcium deficiency

  • Comparing Blossom-end rot (BER) affected tomatoes grown in a low calcium hydroponic solution to healthy fruit grown with a higher calcium hydroponic solution, Mestre et al [2] found a reduction in glutathione content, glutathione reductase activity, and catalase activity

  • Through overexpression of a vacuolar calcium importer, de Freitas et al [5] found that increasing vacuolar calcium and decreasing apoplastic calcium increased BER development in tomatoes. These results suggest that decreased apoplastic calcium can lead to BER development, though the hypothesis that adequate apoplastic calcium incurs a protective effect has not yet been tested

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Summary

Introduction

Blossom-end rot in tomatoes is often used as a model system to study fruit calcium deficiency. The study of blossom-end rot development in tomatoes has been greatly impeded by the difficulty of directly studying and applying treatments to the affected cells. BER is characterized by water-soaking of the tissue and cell death in the blossom-end pericarp. This is followed by blackening and sometimes drying of the affected tissue. Many previous studies on the biological drivers of BER development in tomatoes and peppers have relied on comparing measurements from BER affected fruit to healthy fruit. This approach has identified several possible causes of cell death.

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