AUSTRALIAN PAPAYA DIEBACK - EVIDENCE AGAINST THE CALCIUM DEFICIENCY HYPOTHESIS AND OBSERVATIONS ON THE SIGNIFICANCE OF LATICIFER AUTOFLUORESCENCE

Citation
M. Aleemullah et Kb. Walsh, AUSTRALIAN PAPAYA DIEBACK - EVIDENCE AGAINST THE CALCIUM DEFICIENCY HYPOTHESIS AND OBSERVATIONS ON THE SIGNIFICANCE OF LATICIFER AUTOFLUORESCENCE, Australian Journal of Agricultural Research, 47(3), 1996, pp. 371-385
Citations number
15
Categorie Soggetti
Agriculture
ISSN journal
00049409
Volume
47
Issue
3
Year of publication
1996
Pages
371 - 385
Database
ISI
SICI code
0004-9409(1996)47:3<371:APD-EA>2.0.ZU;2-V
Abstract
The cause of the dieback disorder of Carica papaya (papaya, papaw, or pawpaw) is unknown, although it is a severe problem for the Queensland industry. In this study, the progression of morphological and anatomi cal symptoms during a growing season in Yarwun is documented. Most pla nts which displayed a brown discoloration of the vascular tissue devel oped external symptoms. The discoloration initiated in the stem zone w hich supported leaves, and developed acropetally into the stem apex, a nd basipetally into the trunk and in part of the root system. The disc oloration was autofluorescent under blue or ultraviolet light, and was associated with laticifers in xylem and phloem tissue and in ray pare nchyma. Laticifer autofluoresence was not observed in calcium-deficien t plants, nor in the browning associated with nematode damage, but thi s symptom was present in association with tissue damage caused by Ambl ypelta lutescens (Distant) and in plants suffering root rot. Laticifer discoloration may represent a general stress reaction by the plant. T yloses developed in xylem elements, associated with the wilting of the crown, following development of leaf chlorosis and the bending of the stem tip. Dieback-affected apical tissues were lower in total calcium content than healthy tissues, but were not below an experimentally de termined critical concentration. It is suggested that the low calcium content represents a secondary symptom of the disorder, caused by a ty losis-induced decrease in hydraulic conductivity and consequently in c alcium transport.