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
hypha emerges at the pore, which is driven through the
plant cuticle into the underlying
epidermal cells. The osmotic pressure exerted by the appressorium can reach up to 8 MPa, which allows it to puncture the plant cuticle.[3] This pressure is achievable due to a melanin-pigmented cell wall which is impermeable to compounds larger than water molecules, so the highly-concentrated ions cannot escape from it.[4]
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.[5] 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.[6] Spore adhesion and appressorium formation is inhibited by
hydrolytic enzymes such as α-
mannosidase, α-
glucosidase, and
protease, suggesting that the adhesive materials are composed of
glycoproteins.[6][7] 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.[8]
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', coined the name "appressorium" for the adhesion body formed by the bean pathogen Gloeosporium lindemuthianum on the host surface.[9]
Appressorium development involves a number of steps: nuclear division, first septum formation, germling emergence, tip swelling and second septum formation. 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 appressorium normally contains a single nucleus.[2][10] The outside plasma membrane of the mature appressorium is covered by a melanin layer except at the region in contact with the substratum, where the penetration peg, a specialized hypha that penetrates the tissue surface, develops.[2][11] 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.[12]
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.[18][19]
^Hegde 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): 75–84.
doi:
10.1006/pmpp.1997.0105.
^Deising HB, Werner S, Wernitz M (2000). "The role of fungal appressoria in plant infection". Microbes and Infection / Institut Pasteur. 2 (13): 1631–41.
doi:
10.1016/S1286-4579(00)01319-8.
PMID11113382.
^Bourett TM, Howard RJ (1990). "In vitro development of penetration structures in the rice blast fungus Magnaporthe grisea". Canadian Journal of Botany. 68 (2): 329–42.
doi:
10.1139/b90-044.
^Gilbert RD, Johnson AM, Dean RA (1996). "Chemical signals responsible for appressorium formation in the rice blast fungus Magnaporthe grisea". Physiological and Molecular Plant Pathology. 48 (5): 335–46.
doi:
10.1006/pmpp.1996.0027.
^Correa A, Staples RC, Hoch HC (1996). "Inhibition of thigmostimulated cell differentiation with RGD-peptides in Uromyces germlings". Protoplasma. 194 (1–2): 91–102.
doi:
10.1007/BF01273171.
S2CID8417737.
^Hoch, H. C.; Staples, R. C. (1987). "Structural and Chemical Changes Among the Rust Fungi During Appressorium Development". Annual Review of Phytopathology. 25: 231–247.
doi:
10.1146/annurev.py.25.090187.001311.