2. Spore production under high RH. No spore production
under 89 % RH. Sporulation increases with RH > 93%
Optimun temperature: Sporulation: 25 to 27.7 C
Excessive N fertilizer favours blast
Rice can have blast in all growth stages.
Why and where it occurs…
1st
reported: T.N. (Tanzavore)
Blast can occur wherever blast
spores are present:
low soil moisture, frequent
and prolonged periods of rain
shower
Blast spores
Rice Fever Disease
3. Leaf and collar for lesions: Initial symptoms white to
grey-green lesions or spots, with dark green borders. Older
lesions on the leaves are elliptical or spindle-shaped and
whitish to gray centers with red to brownish or necrotic
border.
Howtoidentify…
Collar blastSpindle-shaped lesions Old lesions
5. One of the most severe diseases of rice.
M. grisea genome size: 40Mb, with approximately 9,000
genes.
The pathogen is a haploid ascomysete that produces
conidia on aerial conidiophores emerging from the center
of lesions.
The conidia consist of three cells. Each conidium
contains an adhesive glycoprotein that, when wet, sticks
tightly to the leaf surface.
The conidium germinates rapidly from one of the
terminal cells and penetrates the leaf surface.
In 4 hours, the apex of the germ tube becomes swollen
and flattened, nucleus divides mitotically, daughter nucleus
migrates into the appressorium being formed at the leaf
surface.
6. Pathogenicity Genes Controlling Production of
Infection Structures
Formation of
specialized infection
cell (appressorium)
Penetrates host
epidermal cell
Appresorium
contains
glycerol
Creates turgor
pressure
(tighmotropic
response)
Penetration peg
punctures host
epidermal cells
M. grisea appresorial wall contains melanin which prevents
glycerol from leackage.
Melanin deficient mutants… unable to generate turgor
pressure…thus NON-PATHOGENIC
7. Melanin synthesis is mediated by several genes…
In M. grisea,
1. Genes for hydrophobin (mpg 1) …………………
appressoria formation
2. Pth 11, used for encoding proteins
embedded in cell membrane………………… host
surface recognition + appressoria formation
Disruption of genes causes reduced pathogenecity
Melanin (dark brown-black pigment): produced by
ascomycetes fungi, polymerized from the polyketide
precursor 1,8-dihydroxynaphthalene. Melanin-deficient
mutants of M. grisea fail to infect intact host plants, but
the same mutants successfully infect plants that have been
wounded by abrading the leaf surface.
8. Extracellular enzymes in penetration
Different cutinases produced by fungal pathogens
functions in pathogenic and saprophytic growth.
Fungal plant pathogens, including M. grisea, have long been
known to secrete enzymes such as cellulases and xylanases
that degrade plant cell walls
Gene disruption techniques now permit an exploration of
the role of these xylanases and other cellwall degrading
enzymes in penetration.
9. Pathogenicity Signaling Genes Used by Plant
Pathogenic Fungi
Fungi use signalling genes, that respond to changes in
the environment, sets off signalling cascades that alter
expression of their genes.
Fungal signalling genes include: G-protein coding genes,
mitogen-activated protein kinase genes etc.
When genes disrupted my mutation, fungi loss all or most of
pathogenecity (growth rate, mating, conidia production, and
toxin production.).
E.g. M. grisea, G-protein genes and MAP kinasen genes
have been cloned and tested through disruption. Several but
not all of the resulting mutants lost pathogenicity.
10. A hydrophobin protein (MPG1) produced in large amounts
during appressorium formation helps appressoria to
recognize hydrophobic surfaces.
The addition of cAMP to the mutants helps in
transmission of surface signal so that appressoria can form
via cAMP. A possible mechanism of transmission of the
signal is through receptor pth11.
Mutants missing Pth11 do not form appressoria and
cannot infect plants.
Role of different genes in pathogenesis…
11. During conidial germination, glycogen and lipids are
degraded and under the control of PMK1, and translocate
rapidly to the germ tube tip.
Gene PLS1 helps in regulation of penetration peg
emergence
Mitogen-activated protein kinases also affect
appressorium morphogenesis.
central signaling pathway: involves the protein PMK1.
that influences appressorium development and mutants of
it cannot produce appressoria or cause infection.
Genes cont….
13. 1.Plant Defense through R genes and their Matching
Avr Genes
The Rice Pi-ta Gene
M. grisea carries the avirulence gene avr-Pi-ta effective
on rice cultivars carrying the resistance gene Pi-ta.
Pi-ta encodes a cytoplasmic protein that contains an NBS
domain and a leucine-rich carboxyl terminus. (1st
experimental evidence of direct interaction of AVR protein
with its R protein).
Protease activity of AVR-Pi-ta is required for its
avirulence function.
How the AVR-Pita/Pi-ta interaction leads to defense
responses is still unknown.
14. Detoxification of toxins, e.g. pyricularin, alpha picnolic
acid, produced by Magnaporthe grisea, in plants plays a role
in disease resistance.
Toxins are metabolized more rapidly by resistant
varieties or are combined with other substances and form
less toxic or nontoxic compounds.
2.Detoxification of pathogen toxins by plants
3. Induction of plant defenses by artificial inoculation
with microbes or by treatment with chemicals (SAR)
Probenazole (synthetic chemical) used for the control of
rice blast disease causes accumulation of salicylic acid
inducing systemic acquired resistance in rice against rice
blast.
15. Seed treatment with Pseudomonas fluroscence
activates the jasmonic acid, ethylene and NO2 Pathways
(mechanism of PR Proteins)
Show strong antifungal by:
Signal compounds: salicylic acid, ethylene, xylanase,
jasmonic acid etc. are responsible for induction of PR
proteins
Among 17 families of PR Proteins, PR1 genes…..
Frequently used as marker genes for SAR.
inhibit spore release and germination
Strengthening of the host cell wall
Treatment with Tricyclazole: Melanin biosynthesis
inhibitors
Melanin deficient mutants… unable to generate
turgor pressure…thus NON-PATHOGENIC
