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muralis (syn. L. muralis ) that were tested for nat-
ural infection with G. cichoracearum , L. serriola
was the most susceptible one. While all L. ser-
riola accessions were highly susceptible to the
disease, L. saligna accessions showed variable
levels of resistance, and accessions of other Lac-
tuca species were mostly resistant or only moder-
ately susceptible (Lebeda 1994). Analysis of the
mapping population developed from the cross
between iceberg-type cv. Salinas and the highly
susceptible L. serriola accession UC96US23
revealed a significant QTL on LG 2 ( pm-2.2 ),
linked to the EST-SSR marker SML-22 (Simko
et al. 2013). The resistance QTL explained up to
40% of the total phenotypic variation of the trait.
Other QTLs were detected on LG 1 ( pm-1.1 ),
LG 2 ( pm-2.1 ), and LG 7 ( pm-7.1 )(Simkoetal.
2013).
iceberg-type cv. Cisco (Michelmore 2010), indi-
cating that cvs. Pavane and Thompson represent
different sources of resistance to big-vein. Resis-
tance genes in accession IVT 280 and cv. Pavane
are different (Hayes and Ryder 2007), thus a
higher level of resistance could be achieved by
combining QTLs from multiple sources.
Fusarium Wilt
Fusarium wilt of lettuce is caused by the fun-
gus Fusarium oxysporum . The disease was first
observed in Japan (Matuo and Motohashi 1967),
but later reported also in Iran, Italy, Taiwan, and
the U.S. (Matheron et al. 2005; McCreight et al.
2005). The first symptoms of the disease are
observed as early as two weeks after seeding
when young plants wilt and die. The incidence
of disease increases as the crop develops.
Infected plants exhibit a distinctive red-brown
streak extending from the taproot into the plant
crown (Hubbard 1997). Three races of the
pathogen are known in Japan, but only race 1
has been detected in the U.S. Resistance to race 1
of the pathogen was observed in the iceberg-type
cvs. Salinas and Salinas 88, and the romaine-like
cv. Costa Rica No. 4, while iceberg-type cv. Van-
guard was highly susceptible (McCreight et al.
2005). Analysis of F 1 and F 2 populations indi-
cated that the resistance in both Costa Rica No. 4
and Salinas is recessive, and that iceberg-type cv.
Calmar is the likely source of resistance in cvs.
Salinas and Salinas 88 (McCreight et al. 2005).
Resistance against F. oxysporum race 1 was
mapped in a population derived from the (Val-
maine
Big-Vein
Big-vein is a viral disease caused by Mirafiori
lettuce big-vein virus (MLBVV) vectored by the
soil-borne fungus Olpidium brassicae (Jagger
and Chandler 1934). This economically damag-
ing disease is distributed worldwide, especially
in areas where lettuce is grown under cool con-
ditions in moist soil (Falk 1997). A partial resis-
tance to big-vein disease was identified in but-
terhead cv. Margarita and Latin-type cv. Pavane,
while L. virosa accession IVT 280 appeared to be
immune (Hayes et al. 2006). However, RT-PCR
(reverse transcription polymerase chain reaction)
analysis demonstrated the presence of the virus
in asymptomatic plants of all three accessions
(Hayes et al. 2008c). A population developed
from crossing susceptible butterhead cv. Parade
with cv. Pavane allowed identification of one
chromosomal region on LG 3 and two regions
on LG 4 that contribute to resistance against big-
vein. The three QTLs together explained 56% of
the observed phenotypic variation (Hayes et al.
2010a; Michelmore 2010). Two different QTLs
were mapped on LG 5 and LG 6 in a pop-
ulation developed from a cross between resis-
tant iceberg-type cv. Thompson and susceptible
Salinas cross (Michel-
more et al. 2010). Three resistance QTLs were
detected on LG 1, LG 2, and LG 7. Resistance
alleles of QTLs on LG 1 and LG 2 originated
from the romaine cv. Valmaine, while resistance
on LG 7 was conferred by the 'Salinas' alleles.
The QTL on LG 2 is linked with the Tvr1 gene
conferring resistance to dieback (Simko et al.
2009, Simko et al. 2010b), however the two resis-
tances do not co-locate absolutely (Michelmore
et al. 2010). Resistance to race 2 of F. oxysporum
×
Salinas 88)
×
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