Investigations on the endogenous activity of gibberellins and cytokinins of malformed mango (Mangifera indica L.) in relation to histological disorders. II. Floral malformation.
Raafat A., El-Deeb S. H., Neumann K. H.
Author Affiliation: Agric. Botany Dept., Faculty of Agriculture, Ain Shams University, Shoubra El-Kheima, Cairo, Egypt.
Angewandte Botanik 69 : 10-16
Abstract : A study on floral malformation in mango was made by examining the anatomical structure of the different parts of terminal twigs of 20-year-old trees of the cultivars Zebda (resistant) and Hindy (susceptible) at the flower bud differentiation stage before the morphological symptoms of the disorder appeared. Parallel to this, assays of gibberellin and cytokinin activities were performed. The shoot apices of Hindy showed earlier differentiation of flower buds than Zebda as manifested by the elongation of the apical meristem and the appearance of lateral branch primordia. The stem of Hindy was characterized by an increased size of the vascular bundle and areas of both phloem and xylem, but with xylem vessels reduced in either number or diameter. This was accompanied by an increased rate of phloem obliteration and the presence of dark companion cells in the functioning sieve elements. All investigated sections showed the absence of inter- or intracellular fungal or bacterial growth in the different tissues. Low GA activity characterized the shoot apex, leaves and stem of Hindy as compared with Zebda, with clear shifting to non-polar GAs in the leaves of Hindy. Gibberellin conjugates were also clearly reduced in the shoot apex and stem of Hindy and were greatly elevated in the leaves. Similarly, cytokinin activity showed lower values in the different parts analysed, especially the shoot apex, of Hindy. The levels of GA activity in healthy Hindy trees were higher than those in malformed ones. It was concluded that a decrease in the gibberellin activity of mango shoot apices, presumably to a critical level readily occurring in low-GA cultivars, could be responsible for the triggering of the malformation syndrome, whatever its original cause.