Growth of plants, in general, is effected by environmental conditions, but its fundamental processes such as cell-division and differentiation operate under the regulation of certain hormonal compounds — auxins (IAA), gibberellins, cytokinins, and ethylene.
Any alteration in the concentration and distribution of these hormonal compounds affects widely the growth physiology of plants. All plant pathogens, to a greater or lesser extent or directly or indirectly, affect the growth and development of their hosts.
Many of the pathogens result in the development of obvious abnormal outgrowths such as galls, tumours, warts, leaf curling, knots, shoot swellings, etc. in their hosts. Such outgrowths are consistent with some alteration in the hormonal status of the host. Evaluation of the role played by individual growth hormones (auxins, gibberellins, cytokinins, and ethylene) in disease development is complex as the physiological effects of these hormones, in many cases, overlap.
Difficulty is also encountered in determining whether any change in hormone levels in due to the accumulation or loss of hormones produced by the host itself or to the production of similar hormonal compounds by the pathogen.
1. Crown gall disease (Agrobacterium tumefaciens) and hairy root disease (A. rhizogenes) are the typical examples. Virulent A. tumefaciens and A. rhizogenes strains possess Ti (tumour-inducing) and Ri (root-inducing) plasmids, respectively. Part of the plasmid is transferred to the plant cell during infection, where it integrates into the host genome. In case of A. tumefaciens (Fig. 8.12), the transferred region (T-DNA) of plasmid carries several genes, which cause the characteristic tumour after their expression in the host cell.
The onc gene direct the synthesis of auxins and cytokinins and lead to uncontrolled division of cell, while other genes direct the synthesis of opines, unusual amino acids, not used by the plant instead catabolized by the pathogen itself. Agrobacterium, therefore, performs the function of a ‘genetic engineer’ by programming host cells to divide uncontrollably, to form galls and then to synthesize opines that serve as a source of carbon and nitrogen for the pathogen.
2. Knot disease of olives, oleander, and privet caused by Pseudomonas syringae pv. sarastanoi is represented by tumour-like outgrowths (knots) formed as a result of unusual cell division, cell enlargement and abnormal differentiation of vascular elements. Studies exploring the pathway for auxin (IAA) synthesis from tryptophan amino acid in olive knot disease convince that the hormones produced by the bacterial pathogen are the main determinants of the symptoms of the disease; genes that code for the two main enzymes involved in the hormone synthesis have now been identified in the pathogen. Auxin (IAA) produced by the pathogen is responsible for tissue proliferation and hence creating a niche in which the pathogen can multiply to high population levels.
3. Increase in cytokinin content has been noticed in diseases such as smut of maize (Ustilago maydis), peach leaf curl (Taphrina deformans), wart of potato (Synchytrium endobioticum), club root of cabbage (PIasmodiophora brassicae), and galls on ornamental plants (Erwinia herbicola). Cytokinins are potent growth hormones mainly associated with the control of cell division. The first cytokinin discovered was kinetin by Scoog and Miller in the early 1950s.
It has been observed that the strains of bacterium Erwinia herbicola pv. gypsophilae that cause galls on ornamental plants (e.g., Gypsophila) secrete considerable amounts of cytokinin in culture. The biosynthesis of cytokinin by the pathogen is attributed to a gene located on a plasmid in a cluster together with genes for auxin biosynthesis. Bacterial strains that do not produce cytokinin due to mutation in cytokinin gene induce much smaller galls in comparison to the pathogenic wild-type strains.
Therefore, it appears that there exists a correlation between cytokinin production and gall disease development by the bacterial pathogen in ornamentals. Chromatographic analysis of the healthy and diseased leaves of peach (Taphrina deformans) has revealed that three cytokinins present in healthy leaves are more active in diseased leaves. Also, an additional cytokinin occurs in diseased leaves but not in healthy ones and this compound, as considered, might be synthesized and secreted by the pathogen.
4. Gibberellins, a group of chemically similar compounds, are the growth regulating hormones occurring as normal constituents of green plants. This class of physiologically active compounds was first identified in culture filtrates of Gibberella fujikuroi, a fungal pathogen that causes ‘bakanae’ or ‘foolish seedling’ disease, which had a devastating effects on the rice economy of Japan during the early part of 20th century. Japanese farmers noted that rice plants affected with this disease outgrew normal plants but were thinner and paler than their normal counterparts and often collapsed.
Plant pathologists concluded that the secretion of gibberellins by the pathogen in the host is the real cause of the disease. Following the classical discovery of the bakanae disease, the first truly experimental investigations on endogenous gibberellins and infected plants were made by Radley in 1961. She showed that nodules in pea roots infected with Rhizobium contain an increased level of gibberellin like substances (GLS) as compared to healthy roots.
5. Ethylene (C2H4), the only gaseous natural plant growth regulator, is biologically highly active. The role of this volatile hormone in disease development is hard to assess as it is produced by plant cells as a natural response to injury and many other conditions of stress. Increased amounts of ethylene are evolved from plant tissues infected by fungi, bacteria, and viruses.
The defoliating symptoms caused by Verticillium wilt of hop plants is attributed to increased levels of ethylene in infected hop plants; the ethylene is considered to act directly as a toxin on plant tissues covering leaf drop, epinasty and premature senescence, and to induce disease resistance in diseased plants.
Many plant pathogens are themselves capable of producing ethylene, but the origin of this volatile hormone in diseased tissues is difficult to determine with certainty.
However, ethylene production by Fusarium oxysporum f. sp. lycopersici causing fusarial wilt of tomato is considered sufficient to account for the epinastic symptoms of the disease. It has been demonstrated that the bacterium Erwinia amylovora does not produce ethylene in culture but when cauliflower florets are inoculated with this bacterium, the latter stimulates ethylene production in the florets.
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