Late Blight of Tomato - Translational Genomics for Crop Breeding: Biotic Stress - page 249

top of the stem or at a node and may progress
down the stem. Firm, brown, and greasy tomato
fruit lesions are often located at the stem end
and sides of green fruit, rendering them unmar-
ketable. Infected tomato fruit may be invaded by
secondary pathogens, causing soft-rot disease.

pathogen attack, plant cells secrete a broad
spectrum of compounds to combat the disease,
including constitutively expressed and inducible
defense-related proteins. These include defense-
related proteins, which function in the degra-
dation of microbial cell walls and inhibiting
pathogen-released elicitors (Foolad et al. 2008;
Hardham and Blackman 2010). Early local-
ized epidermal cell reactions include major rear-
rangements within the cytoplasm leading to
its aggregation beneath the pathogen site, syn-
thesis of ROS, and accumulation of callose
beneath the appressoria within 14 hours after
inoculation or natural pathogen attack (Hard-
ham et al. 2007; Hardham and Blackman 2010)
(Figure 13.1A, B). The rapidly occurring site-
directed cytoplasmic streaming is achieved by
reorganization of cortical and vascular actin
arrays, such that actin microfilaments and cables
form a radial array focused on the infection site.
Subsequently, because of the actin-dependent
focus of cellular secretory apparati (endoplas-
mic reticulum, Golgi bodies, and peroxisomes)
beneath the infection site, a wide variety of
molecules are delivered to the developing cell
wall apposition (Hardham et al. 2007; Hard-
ham and Blackman 2010). Callose, a major
component of the cell wall apposition (Fig-
ure 13.1A, B), alongside other cell wall appo-
sition components, such as phytoalexins, phe-
nolics, silicon, H 2 O 2 , and enzymes such as
peroxidases and enzyme inhibitors, is likely
to inhibit pathogen hyphal penetration. Subse-
quent defense responses include changes in gene
expression and production of phytoalexins and
pathogenesis-related proteins (Hardham et al.
2007; Shibata et al. 2010).
Only after primary host-plant defenses fail
and hyphae successfully penetrate with the for-
mation of haustorium does the plant invoke a
second system of resistance against P. infestans ,
which involves recognition of specific pathogen
molecules and induction of programmed cell
death. HR constitutes a highly effective means
of restricting pathogen growth and its contain-
ment before transition to the necrotrophic phase

Host Plant Defense

Plants are finely tuned to detect the presence of
pathogens on their surface. They perceive both
chemical and physical signals of pathogens and
react rapidly to the attempted infection (Hard-
ham and Blackman 2010; Nowicki et al. 2012).
Possible plant responses to oomycete invasion
vary from invaded cells with no visible response,
to more localized reactions preventing formation
of pathogen intra-cellular structures, to hyper-
sensitive response (HR) and programmed cell
death, the latter occurring only after pathogen
growth had proceeded to the formation of a
clearly identifiable haustorium (Hardham and
Blackman 2010; Hardham et al. 2007).
The primary line of induced defense in tomato
plants against P. infestans is resistance against
penetration at the leaf surface. This is a highly
effective defense strategy rapidly mobilized by
host plants to attempted penetrations (Hardham
et al. 2007). Recent studies have demonstrated
the direct participation of plasma membrane-
bound receptor proteins in the recognition of
apoplastic pathogen elicitors and activation of
host defenses (Haas et al. 2009). Additionally,
the physical pressure exerted by the invading
penetration peg may act as a signal to plant sur-
face detection systems. Triggering of this sys-
tem normally leads to reversible formation of
microfilaments beneath the pressure point within
minutes of the acting stimulus. Both stimuli
may set off the downstream signaling pathways,
including salicylic acid-regulated induction of
cell death, ethylene-dependent production of
phytoalexin, and reactive oxygen species (ROS)-
regulated gene expression and induction of HR
(Haas et al. 2009; Shibata et al. 2010; Now-
icki et al. 2012). In response to the perceived