INVITED REVIEW A Cellular Hypothesis for the Induction of Blossom-End Rot in Tomato Fruit

Background The incidence of blossom-end rot (BER) is generally associated with a calcium (Ca) deficiency in the distal portion of tomato fruits. The visible symptom is a necrotic lesion, which is presumed to be a consequence of cell death and the subsequent leakage of solutes into the extracellular space. Environmental factors that affect either fruit cell expansion or Ca delivery to the distal portion of the fruit influence the occurrence of BER. However, since no absolute, critical fruit Ca concentration for the occurrence of BER has been identified, it is now important to define the role of Ca in fruit cell physiology and to seek the cause of BER at the cellular level. Hypothesis Here, it is suggested that BER is initiated by a cellular dysfunction in the distal portion of a young fruit during rapid cell expansion. It is proposed that insufficient Ca2+ is available for critical apoplastic and cytoplasmic functions when the cellular Ca demand imposed by vacuolation exceeds the Ca delivery to an expanding cell. A local Ca deficiency, therefore, may result in aberrant intracellular Ca2+ signals, a weakening of cell walls and a loss of cellular integrity. Ultimately it may lead to cell death and the visible symptoms of BER. Several experimental strategies are suggested to confirm the occurrence of aberrant Ca2+ concentrations in cells contributing to BER. PerspectiveMany genetic and genomic resources are becoming available for tomato. Ultimately, these will allow genes affecting the occurrence of BER to be identified. Such knowledge will inform breeding strategies to eliminate BER. In the meanwhile, increasing the apoplastic Ca concentration in susceptible fruit tissue should provide a simpl