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Appresoria

An appressorium is a specialized cell typical of many fungal plant pathogens that is used to infect
host plants. It is a flattened, hyphal "pressing" organ, from which a minute infection peg grows
and enters the host, using turgor pressure capable of punching through even Mylar.[1][2]
Following spore attachment and germination on the host surface, the emerging germ tube perceives
physical cues such as surface hardness and hydrophobicity, as well as chemical signals including
wax monomers that trigger appressorium formation. Appressorium formation begins when the tip
of the germ tube ceases polar growth, hooks, and begins to swell. The contents of the spore are
then mobilized into the developing appressorium, a septum develops at the neck of the
appressorium, and the germ tube and spore collapse and die. As the appressorium matures, it
becomes firmly attached to the plant surface and a dense layer of melanin is laid down in the
appressorium wall, except across a pore at the plant interface. Turgor pressure increases inside the
appressorium and a penetration hyphae emerges at the pore, which is driven through the plant
cuticle into the underlying epidermal cells.

Formation
The attachment of a fungal spore on the surface of the host plant is the first critical step of infection.
Once the spore is hydrated, an adhesive mucilage is released from its tip.[3] During germination,
mucilaginous substances continue to be extruded at the tips of the germ tube, which are essential
for germ tube attachment and appressorium formation.[4] Spore adhesion and appressorium
formation is inhibited by hydrolytic enzymes such as -mannosidase, -glucosidase, and protease,
suggesting that the adhesive materials are composed of glycoproteins.[4][5] Germination is also
inhibited at high spore concentrations, which might be due to a lipophilic self inhibitor. Self
inhibition can be overcome by hydrophobic wax from rice leaf.[6]

Uromyces appendiculatus, germ tube and appressorium


In response to surface signals, the germ tube tip undergoes a cell differentiation process to form a
specialized infection structure, the appressorium. Frank B. (1883), in 'Ueber einige neue und
weniger bekannte Pflanzenkrankheiten', first named appressorium as the adhesion body which
was selectively formed by the bean pathogen Gloeosporium lindemuthianum only on the host
surface.[7]
Appressorium development involves a number of steps: nuclear division, first septum formation,
germling emergence, tip swelling and second septum formation. The mitosis first occurs soon after

surface attachment and a nucleus from the second round of mitosis during tip swelling migrates
into the hooked cell before septum formation. A mature appressoria normally contains a single
nucleus.[8][2] The outside plasma membrane of the mature appressorium is covered by a melanin
layer except for the region in contact with the surface of the substratum, where the penetration peg,
a specialized hyphae that penetrates the tissue surface develops.[2][9] Cellular glycerol
concentration sharply increases during spore germination, but it rapidly decreases at the point of
appressorium initiation, and then gradually increases again during appressorium maturation. This
glycerol accumulation generates high turgor pressure in the appressorium, and melanin is
necessary for maintaining the glycerol gradient across the appressorium cell wall.[10]

Initiation
Appressoria are induced in response to physical cues including surface hardness and
hydrophobicity, as well as chemical signals of exogenous cAMP, ethylene, the host's ripening
hormone and the plant cutin monomer, hexadecanoic acid.[11][12] Long chain fatty acids and the
tripeptide sequence Arg-Gly-Asp inhibit appressorium induction.[13][14]
Rust fungi only form appressoria at stomata, since they can only infect plants through these pores.
Other fungi tend to form appressoria over anticlinal cell walls and some form them at any
location.[15][16]

References
1.
Howard RJ, Ferrari MA, Roach DH, Money NP. (1991). "Penetration of hard substrates by a
fungus employing enormous turgor pressures" (PDF). Proceedings of the National Academy of
Sciences 88 (24): 1128184. doi:10.1073/pnas.88.24.11281. PMC 53118. PMID 1837147.
Howard RJ, Valent B. (1996). "Breaking and entering: host penetration by the fungal rice
blast pathogen Magnaporthe grisea". Annual Review of Microbiology 50: 491512.
doi:10.1146/annurev.micro.50.1.491. PMID 8905089.
Braun EJ, Howard RJ. (1994). "Adhesion of fungal spores and germlings to host-plant
surfaces". Protoplasma 181 (14): 20212. doi:10.1007/BF01666396.
Xiao JZ, Ohsima A, Kamakura T, Ishiyama T, Yamaguchi I. (1994). "Extracellular
glycoprotein(s) associated with cellular differentiation in Magnaporthe grisea" (PDF). Molecular
Plant-Microbe Interactions 7 (5): 63944. doi:10.1094/MPMI-7-0639.
Ohtake M, Yamamoto H, Uchiyama T. (1999). "Influences of metabolic inhibitors and
hydrolytic enzymes on the adhesion of appressoria of Pyricularia oryzae to wax-coated coverglasses" (PDF). Bioscience Biotechnology and Biochemistry 63 (6): 97882.
doi:10.1271/bbb.63.978.
Hedge Y, Kolattukudy PE. (1997). "Cuticular waxes relieve self-inhibition of germination
and appressorium formation by the conidia of Magnaporthe grisea". Physiological and Molecular
Plant Pathology 51 (2): 7584.

Deising HB, Werner S, Wernitz M. (2000). "The role of fungal appressoria in plant infection".
Microbes and Infection / Institut Pasteur 2 (13): 163141. doi:10.1016/S1286-4579(00)01319-8.
PMID 11113382.
Shaw BD, Kuo KC, Hoch HC. (1998). "Germination and appressorium development of
Phyllosticta ampelicida pycnidiospores". Mycologia 90 (2): 25868. doi:10.2307/3761301.
Bourett TM, Howard RJ. (1990). "In vitro development of penetration structures in the rice
blast fungus Magnaporthe grisea". Canadian Journal of Botany 68 (2): 32942. doi:10.1139/b90044.
deJong JC, McCormack BJ, Smirnoff N, Talbot NJ. (1997). "Glycerol generates turgor in rice
blast". Nature 389 (6648): 2445. doi:10.1038/38418.
Flaishman MA, Kolattukudy PE. (1994). "Timing of fungal invasion using host's ripening
hormone as a signal". Proceedings of the National Academy of Sciences of the United States of
America 91 (14): 657983. doi:10.1073/pnas.91.14.6579. PMC 44246. PMID 11607484.
Gilbert RD, Johnson AM, Dean RA. (1996). "Chemical signals responsible for appressorium
formation in the rice blast fungus Magnaporthe grisea". Physiology and Molecular Plant
Pathology 48 (5): 33546.
Lee YH, Dean RA. (1993). "cAMP regulates infection structure formation in the plantpathogenic fungus Magnaporthe grisea" (PDF). Plant Cell 5 (6): 693700. doi:10.2307/3869811.
Correa A, Staples RC, Hoch HC. (1996). "Inhibition of thigmostimulated cell differentiation
with RGD-peptides in Uromyces germlings" (PDF). Protoplasma 194 (12): 91102.
doi:10.1007/BF01273171.
Hoch, H. C.; Staples, R. C. (1987). "Structural and Chemical Changes Among the Rust Fungi
During Appressorium Development". Annual Review of Phytopathology 25: 231.
doi:10.1146/annurev.py.25.090187.001311.

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