Electronic Letters to:
|
|
E-letters: Electronic letters published:
-
![[Read eLetter]](/icons/misc/sectionDOWN.gif)
Comments on a cellular hypothesis
- M ax C. Saure (7 February 2006)
|
|
|||
|
M ax C. Saure, retired 21647 Moisburg, Germany
Send e-letter to journal:
|
Dr. Max C. Saure 21647 Moisburg, Dorfstr. 17, Germany phone: +49-4165-6277; fax: -216775 E-Mail: MSaure@t-online.de Date: 2006-02-02 Affiliation: formerly Hannover Chamber of Agriculture; retired Comments on ‘A cellular hypothesis for the induction of blossom-end rot in tomato fruit’, published by Kim C. Ho and Philip J. White in Annals of Botany 95(4): 571-581 (2005). The authors try to defend the established theory that the primary cause of blossom-end rot (BER) of tomato is a local Ca-deficiency in the distal fruit tissue, and that this Ca-deficiency occurs in young, expanding fruit when their demand for Ca exceeds their Ca supply. With this approach, they want to contradict a recent hypothesis that Ca-deficiency is neither a primary nor an independent factor in the development of BER (Saure, 2001). Accordingly, their main recommendation for the prevention of BER is to spray Ca directly onto young fruits, although there are reports that occasionally Ca sprays fail to prevent BER. This is attributed by the authors to an indiscriminate application of the sprays to the entire canopy, without appreciation of fruit development. However, their own experiments with spraying young fruits weekly with 0,5% (w/v) CaCl2 show that even then the incidence of BER may come close to 40% (fig. 5 C), being less than in the unsprayed control but far above what can be tolerated commercially. The authors point to some other observations that as yet are left unexplained by the defended theory: - induction of BER in modern glasshouse tomato production is rarely caused by insufficient Ca in the feed. - BER may occur in plants and fruits with apparently adequate tissue Ca concentrations. - Predicting and preventing the occurrence of BER in glasshouse tomatoes from measurements of their Ca status has not always been effective. In order to solve the problems raised by all these observations, Ho and White emphasize the importance of defining the role of Ca in cell physiology and to seek the cause of BER at the cellular level. However, they do not dispute whether the postulated - but undefined - demand for Ca really exists. In contrary, other authors have argued that young fruits require a low Ca level for rapid cell expansion and high membrane permeability, and that plants have developed mechanisms for restricting the transport of Ca to these organs - with the risk that at high growth rates the tissue content of Ca may fall below a critical level required for cell wall stabilisation and membrane integrity (Marschner, 1995). The restriction of Ca transport appears to be under hormonal control, mainly by gibberellins (GAs) (e.g.Leh, 1963). Obviously, physiologically active GAs themselves can make the fruit cells highly susceptible to stress. Together with high external stress, relative to the degree of susceptibility, this may lead to a deterioration of cell membranes with subsequent loss of turgor and leakage of cell liquids, thus causing the symptoms of BER. Low Ca levels would accompany and promote this effect. Vice versa, factors counteracting the effects of GAs, or interfering with their biosynthesis, may reduce the risk of BER - and contribute to increased Ca levels (cf. Saure, 2005). Therefore, the attempt of the authors to search for a primary and independent role of Ca in BER development is expected to remain futile. References Leh H-O. 1963. Untersuchungen über die Entwicklung von Gibberellin auf Entwicklung, Calcium-Aufnahme und Calcium-Transport einiger Pflanzen. Phytopathologische Zeitschrift 49: 71-83. Marschner H. 1995. Mineral Nutrition of Higher Plants. 2nd edition, Academic Press, Amsterdam. Saure MC 2001. Blossom-end rot of tomato (Lycopersicon esculentum Mill.) – a calcium- or a stress-related disorder? Scientia Horiculturae 90: 193- 208. Saure MC 2005. Calcium translocation to fleshy fruit: its mechanism and endogenous control. Scientia Horticulturae 105: 65-89. Conflict of Interest:None declared |
|||