In addition to the alterations in the normal water economy of the whole plant, many pathogens have ability to alter the normal water relations of individual cells. We know that plasma membrane permeability plays a vital role in inward and outward movement of substances and controls cell water relations in plants.
Plasma membrane is a complex and dynamic structure, which maintains a suitable intracellular environment for metabolism and regulates the passage of ions and organic molecules into and out of the cells. Alterations in permeability have been detected in all diseased tissue examined regardless of the disease type or the nature of the pathogenic agent.
Hutchinson reported the first case of altered permeability in 1913 in tobacco wilt caused by Pseudomonas solanacearum.
Later in 1940s, Thatcher, for the first time, comprehensively studied the extent of permeability alterations in various plant diseases (e.g., powdery mildews, soft rots, dry rots, wilts, rusts) and summarized that:
(1) Fungal pathogen cells possess higher osmotic pressure in comparison to those of their host plants,
(2) Alteration in permeability of the host cells is constantly associated with disease, and
(3) An increase in rust-infected (most-extensively studied) host cell permeability characterizes susceptibility, while decrease in permeability results in resistance in host to the pathogen.
Mechanism of Permeability Alterations:
Mechanisms responsible for alterations in membrane permeability still are not clear. One hypothesis states that toxins combine with some unknown component or receptor in the susceptible cell and thus bring about its disorganization. Phosphatidase, tyrosinase, and pectic enzymes are thought responsible for membrane damage. Hall and Wood (1970) suggest that the rupture of plasma membrane at the site of plasmodermata helps the leakage of electrolytes from endo-PGTE treated tissues.
In has been also advocated that an inducer disrupts the tertiary structure of the membrane protein by breaking the disulphide bond in the bacterial-hypersensitive reactions. Thus, membrane stability and self-repair may be crucial determinative factors in determining susceptibility and resistance. Some phytoalexins have been reported causing damages in plasma membrane.
Permeability Alterations by Necrotrophic Pathogens:
In plant diseases caused by necrotrophic pathogens (e.g., soft rots), wherein the necrosis (cell death) is a major feature, there is pronounced apparent loss in semipermeable property of plasma membrane, and mineral ions and other electrolytes leak out into the external environment. This is predictable as a loss of cellular compartmentalization is likely to place in moribund cells.
Although the actual cause of plasma membrane damage by necrotrophic pathogens is less obvious, it is considered that toxins and hydrolytic enzymes (e.g., pectinases, phospholipase) are the possible culprits for it. The role of toxins in plasma membrane damage has been noted as the primary cause of pathological wilting of plants.
Victorin, a host specific toxin (Pathotoxin), produced by Helminthosporium victoriae in victoria blight of oats, provided a lot of information. A passive leakage of large quantities of electrolytes and increased oxygen uptake was noted in victorin-treated leaf tissues. Stall and Cook (1979) measured the leakage of electrolytes released from leaves of pepper plants inoculated with three races of Xanthomonas campestris pv. vesicatoria, a bacterial pathogen.
They noted that the disruption of plasma membranes and the leakage of electrolytes took place much earlier and at a much greater rate when the leaves were inoculated with bacterial races possessing virulent genes, while release of electrolytes occurred later and at a slower rate with avirulent race of the pathogen.
Permeability Alterations by Bio-Trophic Pathogens:
Bio-trophic pathogens (e.g., pathogens that cause powdery mildews, downy mildews, rusts), which develops haustoria, establish a very specific relationship with the host plasma membrane. Although they increase the permeability of host tissues like necrotrophic pathogens, but they do this without causing any damage to the plasma membrane.
The integrity of plasma membrane is maintained as the cell penetrated by haustoria can be plasmolysed. However, the plasma membrane of the host and the pathogen establish a close associationship particularly near the cell wall penetration site.
As the pathogen haustorium develops, the host plasma membrane becomes invaginated to accommodate the haustorium. This invaginated plasma membrane is called extra haustorial membrane (EHM) and lacks ATPase, membrane bound enzymes responsible to control pumping of H+ ions out and K+ ions in across the membrane.
Nevertheless, there is a definite increase in leakage of electrolytes from diseased tissues, and this change in the semipermeable properties of the plasma membrane is related to the uptake of nutrients by the pathogen. Recent models of haustorial function suggest that the extra haustorial membrane loses control of nutrient transport and the haustoria deplete solutes from the cell matrix surrounding them and maintain a high concentration gradient of solutes in them as the solutes (sugars) pass freely to them.
The significance of membrane system of host cell in the regulation of cell metabolism in diseased condition has only recently been well appreciated. Although the effects of pathogens on plasma membrane is an area of major interest to plant pathologists, the membranes of the organelles (plastids, mitochondria, peroxisomes, lysosomes, etc.) are not less important. Any alterations in one or several of these membrane systems may be involved in many aspects of host physiology.
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