UC Davis

Blossom-end rot is a physiological disorder which causes significant losses in tomatoes, peppers, watermelons, and eggplants. Though blossom-end rot has been associated with calcium deficiency for decades, abiotic and oxidative stress are also significant factors in blossom-end rot development. The cause of cell death during symptom development is not well understood. This dissertation investigates the biological and chemical processes associated with cell death during blossom-end rot development. Due to confounding factors at the whole plant and fruit level, direct treatment and observation of the relevant tissue during blossom-end rot development is difficult. To improve experimentation, chapter 2 demonstrates and validates a new method for studying blossom-end rot using tomato pericarp discs. Chapter 3 uses greenhouse experiments and pericarp disc experiments to investigate blossom-end rot induced by excess calcium application. Chapter 4 uses the pericarp disc system to characterize the importance and timing of calcium and antioxidant related events during blossom-end rot symptom development. Chapter 5 investigates lignification during blossom-end rot as a result of accumulated reactive oxygen species and increased peroxidase activity in whole fruit affected by blossom-end rot. Overall, this research has provided the first causative evidence that calcium, ascorbic acid, and glutathione are protective against BER symptom development. Furthermore, this research shows that calcium and the ascorbic acid-glutathione antioxidant system are directly connected and both reactive oxygen species generation and calcium signaling are critical steps in blossom-end rot induction. Based on these results, the most efficient gains with regards to reduction in commercial blossom-end rot incidence would likely be made through optimizing calcium translocation specifically to the blossom-end pericarp and enhancing the ascorbic acid-glutathione antioxidant system.