Agriculture Reference
In-Depth Information
documented (Evans et al., 1999; Bhathal et al.,
2003).
can be used to distinguish all races of the
pathogen.
Pathogen variability
At the DNA level, genetic variability is extensive
in
Pyrenophora tritici-repentis
, but that level of
variability does not particularly equate to patho-
genic or geographic variability (Friesen et al.,
2005). To determine pathogenic variability,
visible lesion types (necrosis, chlorosis, or both)
were fi rst used to distinguish specifi c pathotypes
and races of
P. tritici-repentis
(Lamari and
Bernier 1989a). Isolates were assigned to four
pathotypes (which later became races 1 through
4) based on their ability to produce necrotic
and chlorotic reactions (race 1), necrosis only
(race 2), chlorosis only (race 3), or neither lesion
type (race 4) on specifi c wheat differential lines
(Lamari and Bernier 1989b). Additional races
were identifi ed as the number of specifi c
P. tritici-
repentis
isolate × wheat differential lines was
expanded and characterized, although race 1 has
been found to predominate in many wheat
growing regions (Lamari et al., 2005; Singh
et al., 2007).
The symptomology produced by specifi c
P.
tritici-repentis
isolates on certain wheat genotypes
was subsequently found to be based on host-
selective toxins produced by the fungus. For races
1 through 8, these toxins produce identifi able
symptoms unique to each isolate-wheat genotype
combination. For example,
P. tritici-repentis
race
1 isolates produced necrotic lesions (due to pro-
duction of toxin Ptr ToxA) on the cultivars
Glenlea and Katepwa; chlorotic lesions (due to
production of Ptr ToxC) on the line 6B365; and
a resistant reaction (no discernable toxin produc-
tion) on 6B662, 'Auburn', and 'Salamouni'
(Lamari et al., 1995; Ciuffetti et al., 1998; De
Wolf et al., 1998; Strelkov et al., 2002; Strelkov
and Lamari 2003). However, further research
showed that some
P. tritici-repentis
isolates did
not have the complement of host-selective toxins
anticipated by the phenotypic race designations
(Andrie et al., 2007). Thus, neither disease phe-
notype nor host-selective toxin genotype alone
FUSARIUM HEAD BLIGHT
Taxonomy and life history
The causal fungus of Fusarium head blight has
the telomorphic stage,
Gibberella zeae
(Schwein.)
Petch, a homothallic ascomycete (Parry et al.,
1995; McMullen et al., 1997). The anamorphic
stage is
Fusarium graminearum
Schwabe. In North
America,
F. graminearum
predominates, whereas
other
Fusarium
species, notably
F. culmorum
,
F.
poae
, and
F. avenaceum
may be found to a lesser
degree in North America or may predominate in
other areas (Sutton 1982; Ireta and Gilchrist
1994). The fungus survives between crops prin-
cipally as mycelia or immature perithecia on
wheat residue (Gilbert and Fernando 2004;
Guenther and Trail 2005). The fungus may also
be found in soil as mycelia, macroconidia, or chla-
mydospores (Nyvall 1970; Bai and Shaner 1994).
Infected seed, whether fallen to the ground during
harvest or planted the following season, may also
serve as a source of inoculum. Because the fungus
also infects maize and rice (
Oryza sativa
L.),
residue from these crops may serve as a source of
inoculum (Sutton 1982; Bai and Shaner 1994).
Ascospores released from perithecia infect wheat
anthers during anthesis, as well as infecting the
wheat glume, palea, and rachis (Bennett 1931;
Pugh et al., 1933; Markell and Francl 2003).
Under favorable conditions, the fungus may
spread throughout the wheat head. Wet, humid
conditions during fl owering are associated with
severe Fusarium head blight (Gilbert et al.,
2008).
Identifi cation and symptomology
The disease is also known as head scab. The
fungus can also contribute to seedling blight, and
to root and crown rot diseases discussed in
Chapter 6. The disease is primarily recognized on
