Introduction to Fungi, Third Edition

596 HETEROBASIDIOMYCETES
Simple appressoria may also be formed. Several
lytic enzymes including cellulases, pectinases
and cutinases are involved in colonizing and
degrading plant tissue.
Another pathogenic species is Rhizoctonia
cerealis (¼ Ceratorhiza cerealis, C. ramicola; teleomorph
Ceratobasidium cornigerum ¼ C. cereale),
which causes sharp eyespot of cereals. As in
R. solani, infection is favoured by cool conditions,
and the disease is more common on winter
cereals than spring-sown varieties. The fungus
overwinters on stubble as mycelium and sclerotia,
and infections give rise to spindle-shaped
eyespot lesions on stems and leaves. These differ
from true eyespot caused by Tapesia yallundae
(p. 439) in being more sharply demarcated, with a
reddish-brown margin enclosing an inner greyish
region. Crop losses in cereals due to R. cerealis are
not generally severe so that chemical control is
not practised specifically against sharp eyespot
(Parry, 1990). Rhizoctonia cerealis also causes yellow
or brown patches in swards of turfgrass, as well
as root and foliar infections in a range of other
crop plants (Kataria & Hoffman, 1988).
Whereas chemical control of Rhizoctonia spp.,
like that of many other soil-borne pathogens, is
difficult, biological control shows some promise.
Several biocontrol organisms are effective under
controlled laboratory and greenhouse conditions,
including species of Bacillus, Serratia and
Streptomyces, as well as 2,4-diacetylphloroglucinolproducing
Pseudomonas spp. (see p. 385). The high
efficacy of Trichoderma spp. against Rhizoctonia has
been partially correlated with their secretion of
cell wall-degrading enzymes, notably chitinases
and b-(1,3)-glucanases (Innocenti et al., 2003;
Markovich & Kononova, 2003). As in the case of
the cereal take-all pathogen Gaeumannomyces
graminis, certain soils can acquire the capacity
to suppress Rhizoctonia after several consecutive
cultivation cycles with the same crop (Henis et al.,
1979; Mazzola, 2002), and this has been attributed
to the build-up of biocontrol organisms, especially
Trichoderma and Pseudomonas spp.
21.2.2 Rhizoctonia and orchid mycorrhiza
Stimulating accounts of this topic have been
written by Arditti (1992), Smith and Read (1997),
Peterson et al. (1998) and Rasmussen (2002).
All members of the plant family Orchidaceae
(about 17 500 species) appear to be associated
with mycorrhizal fungi at all stages of their life
cycle in nature. In contrast to other types of
mycorrhiza, there is a net flow of sugars from the
fungal partner to the plant at least during the
establishment of the orchid seedling. All colourless
(non-photosynthetic) orchids continue to rely
on this external supply throughout their lives,
and even green orchids do not seem to share
their photosynthetic products with the fungus
(Alexander & Hadley, 1985). In orchid mycorrhiza,
therefore, the plant parasitizes the fungus,
and it is a curious fact that many of the fungi
thus exploited are themselves serious plant
pathogens, especially Rhizoctonia spp. (Roberts,
1999). Indeed, the very Rhizoctonia strains isolated
as pathogens of other plants (e.g. R. solani,
R. cerealis) can support the germination of orchid
seeds (Figs. 21.2b f). These as well as other
species (e.g. R. goodyerae-repentis, R. repens) can
also be isolated from mature orchid roots. Orchid
mycorrhizal symbiosis therefore seems to be less
specific than other forms of mycorrhiza
(Masuhara et al., 1993).
Orchid seeds are tiny and lack differentiated
embryos or food reserves. In the absence of soluble
external carbohydrates, they show only
limited germination to form an intermediate
stage called a protocorm. This may emit a few
epidermal hairs before growth stalls (Fig. 21.2b).
Further development of the protocorm (Fig. 21.2c)
occurs only if a suitable soluble carbon source is
added, or if a mycorrhizal fungus such as
Rhizoctonia is allowed to grow from a food base
(e.g. starch or cellulose) to the protocorm. Growth
ensues even if the fungus is made to cross a
barrier between the food base and the protocorms,
thereby demonstrating net carbon translocation
(Smith, 1966). This experiment is easily
set up in the laboratory (Fig. 21.2d; Weber &
Webster, 2001b). The main transport compound
seems to be trehalose, and this may be hydrolysed
to glucose and converted to sucrose by the plant
(Smith, 1967; Smith & Read, 1997).
Infection of the orchid protocorm is initiated
through the epidermal hairs (Fig. 21.2e) or
through the suspensor tissue at the base of