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88 CHAPTER 5

pathogens of insects, discussed in Chapter 15. The

simplest pre-penetration structures are terminal swell-

ings called appressoria (singular: appressorium) if

they occur on germ-tubes, or hyphopodiaif they

develop on short lateral branches of hyphae. More com-

plex infection cushionscan be formed if a fungus

infects from a saprotrophic food base and needs to

overcome substantial host resistance. In these cases

the fungus penetrates from several points beneath the

infection cushion, helping to overwhelm the host

defenses.

All these pre-penetration structures serve to anchor

the fungus to the host surface, usually by secretion of

a mucilaginous matrix. Enzymes such as cutinase

sometimes are secreted into this matrix. The penetra-

tion process is achieved by a narrow hypha, termed

an infection peg, which develops beneath the pre-

penetration structure. There has been much debate

about the relative roles of enzymes and mechanical

forces in the infection process. Enzymes probably are

involved locally, to aid the passage of the penetration

peg through the wall, but they do not cause generalized

dissolution of host walls. Mechanical forces almost

certainly are involved, and have been documented in

detail for Magnaporthe grisea, the fungus that causes rice

blast disease. The penetration pegs of this fungus can

penetrate inert materials such as Mylar and even

Kevlar, the polymer used to manufacture bullet-proof

vests. A turgor pressure of about 8 MPa (mega-Pascals)

is generated in the appressorium of this fungus by the

conversion of stored glycogen into osmotically active

compounds before the penetration peg develops

(Howard et al. 1991). This force is channeled into the

narrow peg because the wall of the upper surface of the

appressorium is heavily melanized and resists deforma-

tion. By contrast, the underside of the appressorium

has a very thin wall, or perhaps none at all, but the

adhesive released by the appressorium is extremely

strong and forms an “O-ring” seal on the host surface

so that the force generated by the infection peg is not

dissipated.

Many appressoria and infection cushions develop

a melanized wall, and this can enable the fungus

to persist on the plant surface until the plant-host

resistance declines. Classic examples of this are found

in Colletotrichumspp. that cause leaf and fruit spots,

including C. musaewhich causes the small brown

flecks on the skins of ripe bananas (Figs 5.3, 5.4).These

fungi are weak parasites that infect fruit tissues only

after the fruit has ripened. But their splash-dispersed

spores can land on the host surface at any time and,

being thin-walled and hyaline (colorless), they cannot

Fig. 5.1Computer simulation of dimorphism in Candida albicans, based on the assumption that wall growth occurs by
bombardment of the wall by apical vesicles generated from a vesicle-supply center (VSC, black dot). The yeast (top
series) and hyphal shapes (lower series) were “grown” simultaneously at the same rate (10,000 vesicles per frame).
Each frame indicates a unit of time. The VSC was moved at different rates to generate the shapes. Between frames 4
and 5 the speed of VSC movement was increased fourfold to produce a cell outgrowth. Then it was returned to its
previous rate to produce the yeast bud, but continued at a fourfold rate to generate the hypha. (Based on Bartnicki-
Garcia & Gierz 1993.)