Agriculture Reference
In-Depth Information
role in disease establishment is not as clear and their significance in pathogenesis is
difficult to establish (Panaccione
et al.
, 2002). Nevertheless, as shown by disruption
experiments in which toxin synthesis has been negated, non-specific toxins may
contribute to virulence.
A very well studied example of a non-host toxin is cercosporin produced by
several species of the genus
Cercospora
causing leaf spot diseases on a diversity of
crop species world-wide. Cercosporin is a photosensitising compound that has been
shown to be toxic not only to plants but also to mice, bacteria and many species of
fungi (Daub and Ehrenshaft, 2000). Nevertheless, the role of cercosporin in
pathogenicity is not clarified. First evidence came from
C. kikuchii
mutants deficient
in cercosporin production. Inoculation of soybean with these mutants resulted in
reduced virulence (Upchurch, 1991). In addition, only recently, a functional and
molecular characterisation of a polyketide synthase was presented that is involved in
cercosporin biosynthesis. Virulence of these mutants is also markedly reduced
(Choquer
et al.
, 2005).
In contrast, the host-selective toxins, most of which are produced by species of
the genera
Alternaria
and
Cochliobolus
, are determinants of specificity (for review,
see Markham and Hille, 2001; Wolpert
et al.
, 2002). The function of some of these
compounds is regulated by single host plant genes (Walton, 1996), making them
ideal subjects for examining host-parasite specificity.
Examples of
Cochliobolus
toxins are HC-toxin (Walton
et al
., 1997), synthesized
by races of
C. carbonum
that cause leaf spot disease of maize; T-toxin, synthesised by
C. heterostrophus
causing Southern Corn Leaf Blight disease (Dewey
et al.,
1988;
Rose
et al.
, 2002), and victorin synthesised by
C. victoriae
responsible for Victoria
blight disease in oats (Meehan and Murphy, 1946; Navarre and Wolpert, 1999; Curtis
and Wolpert, 2004)
.
The cellular targets and possible mechanisms are divers.
However, in most cases these toxins as well as the
Alternaria
toxins kill the plant cells
of their specific host plants and enable the fungus to spread throughout the host tissue,
with one exception: the HC-toxin does not kill the host cells but is able to prevent the
plant defence reaction. HC-toxin is a cyclic peptide functioning as an inhibitor of
histone deacetylase (HDAC) from many organisms. As a result, the hyperacetylated
form of histon is accumulated. It is supposed that this leads to the inhibition of the
synthesis of plant defense proteins (Brosch
et al.
, 1995; Ransom and Walton, 1997).
However, the activities and roles of phytotoxins in different pathosystems are
highly variable. Most of them are clearly involved in virulence. In contrast, the so-
called NIP2 protein from
Rhynchosporium secalis
that was originally detected as a
non-specific phytotoxin inducing necrosis of barley leaves (Wevelsiep
et al.
, 1993) has
been shown to function as an elicitor in the recognition process of plants carrying the
Rrs1 resistance gene. As a result plants react with the onset of the defence response.
Consequently, NIP1 functions as an avirulence determinant (Rohe
et al.
, 1995).
4.4.2 Biotrophs
Plant-infecting biotrophic fungi have developed an intimate relationship with their
host plants. In contrast to necrotrophs, these fungi colonize and draw nutrients only
