Biology Reference
In-Depth Information
biotrophic growth phase, nutrients are obtained
from living plant cells. This is achieved by form-
ing a penetration peg, which pierces the cuticle
and enters an epidermal cell to form an infection
vesicle (Figure 13.1A, B). Formation of digit-
like haustoria (i.e., appressoria-like structures)
by the branching hyphae, and the subsequent
secretion of enzymes that degrade components
of the plant cell wall further facilitate the nutrient
access. Haustoria, specialized for nutrient uptake
from the host cell, develop within the bound-
ary of the plant cell wall, although they remain
outside the host cell plasma membrane (Hard-
ham and Blackman 2010). This is followed by
extensive necrosis of host tissue resulting in col-
onization and sporulation. During necrotrophic
growth, nutrients required for pathogen growth
and reproduction are obtained from dead and
dying cells in the necrotic lesions that develop as
the pathogen colonizes the plant. As the infected
tissue necrotizes, the mycelium develops spo-
rangiophores that emerge through the stomata to
produce numerous asexual sporangia (Hardham
and Blackman 2010; Nowicki et al. 2012) (Fig-
ure 13.1C, D).
P. infestans
preferentially sporulates
in planta
during dark periods. Studies have demonstrated
that continuous light inhibits sporulation (Now-
icki et al. 2012). As there is no evidence for
a light-regulated clock in the pathogen (Raf-
faele et al. 2010b), this suggests that a plant-
derived signal generated by the day-night cycle
influences sporulation. Similar phenomena are
common among the oomycetes (Judelson et al.
2009; Hardham and Blackman 2010). At the
plant surface,
P. infestans
zoospores maneuver
such that their ventral surface faces the plant
before the flagella are detached and proteins from
three different cortical vesicles are secreted onto
the zoospore surface (Hardham and Blackman
2010). By doing so, the spores form walled cysts,
which germinate from the center of the ven-
tral surface, allowing the hyphae to grow along
the anticlinal walls between epidermal cells to
form appressoria for breaching plant cells (Fig-
ure 13.1A, B). Under favorable conditions, the
multinucleate sporangia can also initiate infec-
tions. Mature sporangia can preemptively syn-
thesize the proteins involved in zoosporogenesis
and encystment (Nowicki et al. 2012).
In general, during infection, phytopathogens
secrete peptides and proteins, broadly known
as effectors (Raffaele et al. 2010b; Vleeshouw-
ers et al. 2011). Effectors can be of two types:
apoplastic effectors, which target the extracellu-
lar space, and cytoplasmic effectors, which tar-
get subcellular compartments. Effectors include
enzymes involved in degrading the plant cell
wall and suppressing extracellular plant defenses
(Vleeshouwers et al. 2011; Hardham and Black-
man 2010; Nowicki et al. 2012). In-depth discus-
sion of these proteins in
P. infestans
pathogenesis
is presented in the potato LB chapter (Chapter 12
in this volume), as major advances in this field
have been achieved in research on this host plant.
Disease Symptoms and Progression
P. infestans
can quickly devastate tomato and
potato crops at any time during plant ontogeny.
The entire plant may collapse in five to ten days.
LB can infect all aboveground parts of the plant,
causing leaf and stem necrosis, fruit rot, and
eventual plant death (
http://www.nysipm.cornell
.edu/publications/blight/).
The pathogen can
also infect tomato seed and potato tubers (Rubin
et al. 2001; Nowicki et al. 2012). Initial infection
symptoms, including small lesions on leaf tips
and plant stems, are visible only after three
to four days, and in some cases reach only 1
to 2 mm in diameter. The purple, dark brown,
or black water-soaked lesions often have a pale
yellowish-green border that blends into the
healthy tissue. As the pathogen penetrates the
plant tissue, lesions enlarge in size (
http://www.
light_tomato.htm). Fl
uffy, white sporangia may
grow on the lower (abaxial) leaflet surface in
moist weather. As the disease progresses, plant
leaflets shrivel and die and the disease spreads to
the rest of the foliage, leading to extensive defo-
liation. Dark brown LB lesions first appear at the
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