Biology Reference
In-Depth Information
resistant to corky root were identified. However,
it has not yet been determined if these accessions
harbor a new resistance gene, because genotyp-
ing with markers ( SCY15 and SC853 ) flanking
the cor gene was not conclusive.
quently used in the European breeding programs
(Pink et al. 1992), while the mo-1 2 allele was
used to develop LMV-resistant cultivars in the
USA (e.g., Salinas 88, and Vanguard 75) (Ryder
1979; Ryder 1991). Sequencing of the mo-1 gene
confirmed that the mo-1 1 and mo-1 2 are alle-
les of the same gene that is coding the eukary-
otic translation initiation factor (eIF4E) (Nicaise
et al. 2003). Nucleotide difference between the
two resistant alleles and the susceptible Mo-1
allele allowed development of molecular mark-
ers that distinguish among all three alleles and
can be used in MAS (Appendix). Strains of
LMV (pathotype IV) have been identified that
overcome resistance based on mo-1 1 and mo-1 2
alleles (Pink et al. 1992). This LMV pathotype
from Spain has never been reported in the USA.
The Mo-3 gene from L. virosa appears to pro-
vide efficient protection against all LMV iso-
lates breaking resistance based on mo-1 , includ-
ing pathotype IV (Maisonneuve et al. 1999).
A gene conferring a mild systemic reaction to
LMV in its dominant stage was described and
named Mi (Ryder 2002). Combining the mo-1
gene and the Mi gene raises the level of lettuce
resistance to nearly complete (Ryder 2002). The
position of the Mi gene on the molecular linkage
is not known, and an assay for MAS has not been
developed.
Lettuce Mosaic
Lettuce mosaic is caused by Lettuce mosaic virus
(LMV) from the family Potyviridae .LMVis
one of the most serious viruses attacking let-
tuce crops worldwide. The virus is seed-borne
and highly transmissible by aphids (Candresse
et al. 2006). Leaves of infected plants show
symptoms of mosaic (Figure 14.2C) and their
growth is greatly reduced. Severely infected and
stunted plants do not form heads, thus making
them unmarketable. Prevention of disease out-
break is mainly based on the use of virus-free
seeds, management of aphids, and growing resis-
tant cultivars. Four genes have been reported that
confer resistance to LMV; one recessive gene
( mo-1 ) and three dominant genes ( Mo-2 , Mo-3 ,
and Mo-4 ) (Candresse et al. 2006). The dominant
genes are currently not used in breeding pro-
grams because of their limited durability ( Mo-2 )
(Pink et al. 1992), or the difficulty of introgress-
ing genes from L. virosa ( Mo-3 and Mo-4 )into
cultivated lettuce (Le Gall et al. 1999; Maison-
neuve et al. 1999; Candresse et al. 2006). The
position of the Mo-3 and Mo-4 genes on the
molecular linkage map is not known; the Mo-
2 gene that was first identified in crisp-type cv.
Ithaca (Pink et al. 1992) is located on the LG 1
(McHale et al. 2009) (Table 14.1).
The recessive mo-1 gene is usually associated
with tolerance or resistance to LMV (Dinant and
Lot 1992), depending on the virus isolate and
genetic background of the plants (Pink et al.
1992; Revers et al. 1997). Two alleles of the
mo-1 gene that is located on LG 4 (Nicaise et al.
2003) were originally identified in cv. Gallega
de Invierno ( mo-1 1 ) (von der Pahlen and Crnko
1965) and the L. sativa accession PI 251245
( mo-1 2 ) (Ryder 1970). The mo-1 1
Lettuce Dieback
Lettuce dieback is a soil-borne disease caused
by two closely related viruses from the fam-
ily Tombusviridae - Tomato bushy stunt virus
(TBSV) and Lettuce necrotic stunt virus (LNSV)
(Obermeier et al. 2001). The mechanism of virus
transfer to plants is yet unknown. The disease is
widespread in all types of commercially grown
lettuce with the exception of modern iceberg-
type cultivars. Symptoms of this disease include
mottling, yellowing, and necrosis of older leaves,
and stunting and death of plants (Figure 14.2D),
leading to complete loss of the crop in a severely
infected field. The disease has been observed
allele is fre-
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