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STRUCTURAL DEFENSE MECHANISMS
POST-INFECTIONAL STRUCTURAL DEFENSE MECHANISMS
S.G.S.HarshanaAG/2011/2012/160Faculty of AgricultureRajarata University of Sri Lanka
PLANT RESISTANCE MECHANISM
• STRUCTURAL DEFENSE
• BIOCHEMICAL DEFENSE
Pre-existing structural defense mechanism
Post infectional structural defense mechanism
POST INFECTIONAL DEFENSE MECHANISM (INDUCED/ACTIVE)
• Occurs once after the infection of a plant by a pathogen.
• The activation or induction of defense mechanism may be both specific and
non-specific type.
• Several structural changes are known to be induced by a range of biotic or
abiotic elicitors.
• These dynamic defense mechanisms prevent further colonization or spread of
pathogen.
• Four types of induced/active structural defense mechanisms,
• Histological defense structures
• Cellular defense structures
• Cytoplasmic defense structures
• Hypersensitive/ Necrotic defense reaction
HISTOLOGICAL DEFENSE STRUCTURES
• Even after the establishment of infection in plant cells, the host defense system
tries to create barriers for further colonization of tissues. This may be at various
levels.
1. Lignification
• Lignified cell wall provide effective barrier to hyphal penetration.
• They also act as impermeable barrier for free movement of nutrient causing starvation
of pathogen.
• Examples:
Radish: Peronospora parasitica, Alternaria japonica
Potato: Phytophtora infestans
Wheat: Septoria nodorum
Cucumber: Cladosporium cucumerium, Colletorichum lagenarium
Carrot: Botrytis cineria
2. Suberization
• In several plants the infected cells are surrounded by suberized cells.
• Thus, isolating them from healthy tissue. corky layer formation is a part of
natural healing system of plants.
• Examples : Common scab of potato
3. Abscission layers
• Gap between host cell layers and devices for dropping –off older leaves and
mature fruits.
• Plant may use this for defense mechanism also. I.E. To drop-off infected or
invaded plant tissue or parts, along with pathogen.
• Shot holes in leaves of fruit trees is a common feature.
• Occurred due to the infection of fungi, bacteria, and viruses.
4. Tyloses
• Formed by protrusion of xylem parachymatous cell walls, through pits, into
xylem vessels.
• The size and number of tyloses physically block the vessel.
• The tyloses are inductively formed much ahead of infection, thus blocking
the spread of pathogen.
• It suggests biochemical elicitors and movement of tyloses inducing facto
(TIF) up the stem.
• Examples :
Sweet potato: Fusarium oxysporum f. Sp. batatas.
5. Gum deposition
• The gums and vascular gels quickly accumulate and fill the intercellular
spaces or within the cell surroundings the infection thread and haustoria,
which may starve or die.
6. Hyphal sheathing
• The fungal hyphae, which penetrate the cell wall are often unsheathed by
the extension of the cell wall.
• This delays contact between hypha and protoplasm.
• Later on, the hyphae penetrate the sheath and invade the lumen of the cell.
INDUCED CELLULAR DEFENSE STRUCTURES
• The cellular defense structures, I.E. Changes in cell walls, have only a limited
role in defense.
• Following types are commonly observed.
• Carhohydrate apposition (synthesis of secondary wall and papillae formation)
• Callose deposition (hyphal sheathing just outside plasma lemma around the
haustorium which delays contact of pathogen (Phytophythora infestans) with host
cells.
• Structural proteins
• Induced cytoplasmic defense that present last line of host defense and may effective
against slow growing pathogens, weak parasites or some symbiotic relationship.
CYTOPLASMIC DEFENSE STRUCTURES
• In a few cases of slowly growing , weakly pathogenic fungi that induce chronic
diseases or nearly symbiotic conditions , the cytoplasm surrounds the clump of
hyphae , and the nucleus is stretched to the point where it breaks in two .
• In some cells , the cytoplasmic reaction is overcome and the protoplast
disappears while fungal growth increases .
• In some of the invaded cells , however , the cytoplasm and nucleus enlarge .
• The cytoplasm becomes granular and dense , and various particles or structures
appear in it.
• Finally , the mycelium of the pathogen disintegrates and the invasion stops .
HYPERSENSITIVE/NECROTIC DEFENSE REACTION
• When the pathogen penetrates the cell wall, and establishes contact with the
protoplast of the cell, the nucleus of the cell moves toward the intruding
pathogen soon disintegrates forming resin-like brown granules in the
cytoplasm.
• Firstly, all the granules are formed around the pathogen and then throughout
the cytoplasm.
• Simultaneously the cell walls swell.
• As the browning of the cytoplasm continues and the necrosis is caused, the
invading hypha begins to disintegrate, and the further invasion of the pathogen
is stopped.
• Common in diseases caused by obligate fungal parasites, viruses and
nematodes.
• The necrotic tissue isolates the obligate parasite from the living substances and
the death is caused to the pathogen because of starvation.
REFERENCES
• Pandey, B.P. And P, B.P. (2001) plant pathology: pathogen and plant disease. India: S
chand & co.(Pandey and P, 2001)
• Deverall, B.J. (1977). Defense mechanisms of plants. Cambridge university press.
• Brown, j.F. (1980). Mechanisms of resistance in plants to infection by pathogens, n J. F.
Brown (ed.) Plant protection pp. 254-266. Australian vice-chancellors' committee,
canberra.
• Agrios, G.N. (2005) plant pathology. 5th edn. Amsterdam: elsevier academic press.
(Agrios, 2005)
• Society, T.A.P. (2016) welcome to APS. Available at:
http://www.Apsnet.Org/pages/default.Aspx (accessed: 24 october 2016).