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AOBPreview originally published online on January 10, 2005
Annals of Botany 2005 95(4):571-581; doi:10.1093/aob/mci065
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Annals of Botany 95/4 © Annals of Botany Company 2005; all rights reserved

INVITED REVIEW

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

LIM C. HO and PHILIP J. WHITE*

Warwick HRI, Wellesbourne, Warwick CV35 9EF, UK

* For correspondence. E-mail philip-j.white{at}warwick.ac.uk

Received: 2 September 2004    Returned for revision: 19 October 2004    Accepted: 19 November 2004    Published electronically: 10 January 2005

• 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.

• Perspective Many 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 simple and reliable, practical solution for the prevention of BER in tomatoes. It is suggested that current horticultural practices, such as the manipulation of the mineral composition of the feed or the growth environment, are not completely effective in reducing BER because they affect apoplastic Ca concentration in fruit tissue indirectly. Therefore, spraying Ca directly onto young fruits is recommended for the prevention of BER.

Key words: Annexin, blossom-end rot (BER), calcium (Ca2+), environmental conditions, fruit, mineral nutrition, phloem, tomato (Lycopersicon esculentum), xylem


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Comments on a cellular hypothesis
M ax C. Saure
Annals of Botany, 7 Feb 2006 [Full text]

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