Biological control agents in plant disease control - Disease Control in Crops - page 31

and then degradation (Chet et al ., 1998; Steyaert et al ., 2003; Lu et al ., 2004). Numerous
variations on the basic process exist. For example, the production of haustoria in the
biotrophic phase of infection by the BCA Verticillium biguttatum during parasitism of
Rhizoctonia solani hyphae (van den Boogert & Deacon, 1994), intracellular growth
by Ampelomyces quisqualis in powdery mildew hyphae (Kiss et al ., 2004) and inter-
or intracellular growth of BCA hyphae of many mycoparasites during infection of
complex propagules such as sclerotia (Jeffries & Young, 1994; Rey et al ., 2005), but cell
wall degrading enzymes always seem to be involved in the process. Molecular proof of
the involvement of specifi c extracellular enzymes is diffi cult to obtain for some myco-
parasites due to the presence of multiple copies of similar genes where knock-out of one
gene leaves others functional, despite potentially having a role in the parasitism process
(Carsolio et al ., 1999; Woo et al ., 1999; Grevesse et al ., 2003). Nevertheless, through
some molecular expression studies, gene knock-out experiments and microscopical
cytochemical labelling procedures, along with a history of correlative studies, involve-
ment of chitinases, glucanases, proteases and cellulases seems clear (Benhamou & Chet,
1996; Baek et al ., 1999; Rotem et al ., 1999; Markovich & Kononova, 2003; Steyaert
et al ., 2003; Pozo et al ., 2004; Rey et al ., 2005; Morissette et al ., 2006; Woo et al ., 2006;
Friel et al ., 2007). Earlier, directed growth was thought to refl ect growth along a chemi-
cal gradient of amino acids and sugars but recent evidence in Trichoderma spp. suggests
that low level expression of cell wall degrading enzymes by the BCA leads to the release
of low-molecular-weight oligosaccharides from the host cell wall that in turn are recog-
nised by Trichoderma , resulting in stimulated growth, antibiotic and enzyme production,
and mycoparasitism (Viterbo et al ., 2002; Brunner et al ., 2003; Zeilinger et al ., 2003;
Woo et al ., 2006). On contact, the recognition and coiling appear to be lectin mediated
(Barak et al ., 1985). Recent molecular studies suggest that the G subunit of heterotri-

meric G proteins plays a role in the signal transduction to increase chitinase expression,
antibiotic production and coiling during mycoparasitism (Rocha-Ramirez et al ., 2002;
Mukerjee et al ., 2004; Reithner et al ., 2005). Mitogen-activated protein kinase (MAPK)
cascades may also be involved in mycoparasite signal transduction in Trichoderma but
may differ in response with isolate, host and environment (Mendoza-Mendoza et al .,
2003; Mukherjee et al ., 2003). Enhanced antagonistic effects may consequently occur
in Trichoderma through combined action of cell wall degrading enzymes with different
target polysaccharides or through combination with release of antibiotics (Schirmbock
et al ., 1994). However, recent studies suggest that for some Trichoderma isolates, modes
of action involving interactions with the plant may be more signifi cant than previously
thought (Harman et al ., 2004; Howell, 2006).
Production of extracellular enzymes that degrade virulence factors such as N -acyl
homoserine lactones have been mentioned previously as a mode of action involved
with regulation of antibiotic production (Molina et al ., 2003; Dong et al ., 2004) but this
general concept is growing in importance. For example, Pantoea dispersa produces an
esterase that detoxifi es the toxin albicidin produced by Xanthomonas albilineans (Zhang
& Birch, 1996, 1997) and Trichoderma harzianum produces proteases that degrade
hydrolytic enzymes produced by Botrytis cinerea on bean leaves, preventing the pathogen
from infecting its host (Kapat et al ., 1998; Elad & Kapat, 1999). A related concept is
detoxifi cation of virulence factors rather than their degradation. For instance, detoxifi ca-
tion of albicidin by proteins produced by Klebsiella oxytoca (Walker et al ., 1988) and

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