Late Blight of Tomato - Translational Genomics for Crop Breeding: Biotic Stress - page 250

occurs (Vleeshouwers et al. 2000; Hardham et al.
2007). Elicitins and effectors are the two main
groups of molecules that induce HR. Upon their
being recognized by host plants, elicitins induce
HR. For instance, P. infestans INF1 elicitin ini-
tiates cell death upon interaction with the lectin-
like receptor kinase NbLRK1 in N. benthamiana
(Hardham et al. 2007; Kanzaki et al. 2008). In
total, genes coding for seven avirulence effec-
tor proteins of P. infestans have been cloned at
present (Vleeshouwers et al. 2011; van Damme
et al. 2012), and all of them are recognized by
cytoplasmic nucleotide-binding site/leucin-rich
repeat (NBS-LRR) receptors (Jia et al. 2010;
Vleeshouwers et al. 2011) encoded by the plant
resistance ( R )-genes. Race-specific and broad-
spectrum R -genes in host plants induce a sim-
ilar set of defense reactions as a response to
recognition of their corresponding P. infestans
avirulence factors, the effector proteins (Shibata
et al. 2010; Nowicki et al. 2012). In tomato,
a wide range of proteins secreted by P. infes-
tans and the host plant during a compatible
interaction was identified in an in planta secre-
tome study using the yeast secretion trap tech-
nique (Lee et al. 2006). Almost half the secreted
proteins in the tomato plants had known asso-
ciations with defense, including pathogenesis-
related (PR) proteins, structural proteins, gly-
cosyl hydrolases (which target glucans, typical
constituents of microbial cell walls), and a puta-
tive peroxidase. Other secreted proteins had less
defined roles in defense, including those induced
by wounding or elicitors. Additionally, about one
third of the induced genes had no obvious func-
tional domains or homology to known genes (Lee
et al. 2006).
To date, no mechanisms for LB resistance
have been proposed in either tomato or potato.
A preliminary study was conducted to elucidate
the mechanism of vertical LB resistance con-
ferred by the S. bulbocastanum R -gene, RB ,by
investigating the effects of RarI and SgtI on LB
resistance (Bhaskar et al. 2008). Unlike the resis-
tance conferred by most major genes, RB slows
disease progress but does not eliminate disease

symptoms (see Chapter 12 of this volume). RarI
and SgtI are known to regulate R -genes' expres-
sion. Although proposed to be involved in form-
ing or stabilizing R-protein associated recogni-
tion complexes, silencing RarI using RNAi had
no effect on RB resistance, indicating that it is
not required in the LB-resistance response. Con-
versely, silencing Sgt1 , known to be involved in
NBS-LRR and Pto-kinase mediated resistance,
resulted in disease susceptibility, indicating that
SGT1 plays a role in LB resistance (Shibata et al.
2011). Another study on phenotypic characteri-
zation of potato LB resistance conferred by RB
suggests that expression of HR and PR genes may
play a critical role in the resistance response,
with callose deposition being negatively corre-
lated with resistance levels in tested plants (Chen
and Halterman 2011).
Collectively, multiple defense mechanisms
seem to be involved in LB resistance and alter-
ation of metabolic pathways may be one of
the most important disease defense responses
(Bhaskar et al. 2008; Foolad et al. 2008;
Chen and Halterman 2011). Nevertheless, innate
tomato-derived LB-resistance mechanisms alone
may not suffice to defend the plants against the
aggressive pathogen, hence the need to integrate
various protection methods into crop production.

LateBlight Disease Control

Tomato and potato LB are of significant fiscal
importance to growers and consumers world-
wide, costing approximately US$5 billion annu-
ally, including the cost of disease control and
crop losses (Foolad et al. 2008). In the United
States, in 2009 total yield losses for fresh-
market and processing tomato industries reached
US$46 million and US$66 million, respectively
(USDA 2011). Of these losses, up to half could
be attributed to crop losses resulting from LB
(Haverkort et al. 2008; Nowicki et al. 2012).
In tomato, fruit infection may range from 41 to
100% in unprotected fields and from 12 to 65% in
plots protected with systemic fungicides (Now-
icki et al. 2012). Polish tomato production has