Late Blight of Tomato - Translational Genomics for Crop Breeding: Biotic Stress - page 253

by airborne spores over long distances (Scott
and Gardner 2007). Conversely, race-specific
major resistance genes have been useful in breed-
ing tomatoes for resistance against LB, and in
fact against many other tomato diseases (Foolad
2007). Further, many major resistance genes
have shown durability and been very useful for
breeding purposes in other crop species. The use
of major disease resistance genes, however, has
been shown to be most effective when multiple
resistance genes are pyramided; this approach
often increases resistance strength and durabil-
ity (Kim et al. 2012; Luo et al. 2012). Thus, it
is prudent to identify additional major resistance
genes against tomato LB, a task that is underway
in many tomato-breeding programs around the
world (Merk and Foolad 2011, Merk et al. 2012;
Nowicki et al. 2012).

of chromosome 7 using morphological markers
(Pierce 1971). Subsequently this resistance trait
was incorporated into the old processing tomato
cv. 'Nova' and the old fresh market tomato cv.
'New Yorker'. Since T 0 is no longer the predomi-
nant race of P. infestans , and since Ph-1 has been
long overcome by new aggressive pathogen lin-
eages, this LB-resistance source is no longer con-
sidered useful for tomato breeding (Foolad et al.
2008; Nowicki et al. 2012). Currently, cultivars
containing Ph-1 exhibit complete susceptibility
to LB.
A second tomato LB-resistance gene named
Ph-2 was identified in an S. pimpinellifolium
accession known as West Virginia 700 (Gallegly
and Marvel 1955) and subsequently mapped
to the long arm of tomato chromosome 10
between markers CP105 and TG233 (Moreau
et al. 1998) (Figure 13.2A). There has not been
any further effort to fine map or clone Ph-
2 (N. Grimsley, CNRS-INRA, personal com-
munication). Incompletely dominant LB resis-
tance conferred by Ph- 2 provides only partial
resistance against several pathogen isolates and
confers only a reduction in the rate of disease
development, rather than blocking the disease.
Furthermore, Ph-2 often fails in the presence
of more aggressive P. infestans isolates. Charac-
terization of this resistance has been hampered
because its expression is partially dependent
upon environmental conditions, plant physiolog-
ical age, the organ assessed, and the pathogen
isolate used (Moreau et al. 1998). Despite these
shortcomings, Ph-2 has been successfully incor-
porated into a number of named fresh-market and
processing tomato varieties, including Legend,
Centennial, Macline, Pieraline, Herline, Fline,
Flora Dade, Heinz 1706, Campbell 28, and
Europeel (Gallegly 1960; Nowicki et al. 2012).
Recently a few PCR based markers associated
with Ph-2 have been identified (M. Mutschler,
personal communication), which are being used
for development of breeding lines and hybrid
cultivars of tomato containing Ph-2 . Neverthe-
less, virulence variability observed in P. infestans
has made this source of tomato resistance less

Identification of Resistance
Resources and Breeding for
LBresistance in Tomato

Overview of Early Studies of
LB Resistance

Following an LB outbreak in the U.S. in 1946,
which affected potatoes and tomatoes, a sub-
stantial amount of research was initiated to
locate sources of genetic resistance in tomato
(Bonde and Murphy 1952; Gallegly and Mar-
vel 1955; Gallegly and Galindo 1958; Gallegly
1960). Such research led to the discovery of
resistant accessions within wild tomato species,
in particular S. pimpinellifolium (Gallegly and
Marvel 1955). The first reported tomato LB-
resistance gene, Ph-1 , a completely dominant
gene conferring resistance against P. infestans
tomato race-0 (T 0 ), was originally located in
S. pimpinellifolium accessions known as West
Virginia 19 and 731 (Bonde and Murphy 1952;
Gallegly and Marvel 1955; Pierce 1971). An
LB-resistant cultivar containing Ph-1 , Rocking-
ham, was released in 1962 (Rich et al. 1962).
This cultivar was subsequently used to map the
gene conferring LB resistance to the distal end