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phenotypic variance and QTLs alleles for increased oil were transmitted by
the oilseed parent (RHA801). Five QTLs were identified on LG 5, 9, 10, 14,
and 17 for 100-seed weight. The QTLs collectively explained 73.4% of the
phenotypic variability. The RHA280 allele from four of the five QTLs
increased 100-seed weight, whereas the RHA280 allele for one of the five
QTLs decreased 100-seed weight. Results showed that three QTLs on LG 9,
10 and 17 control both the traits. An apical branching loci (B) and a
phytomelanin pigment loci (P) were linked to a QTL, which control both the
traits on LG 10 and 17, respectively. The B -liked QTL, which is located on
linkage 10, explained 22.5% and 52.5% of phenotypic variation for seed oil
concentration and 100-seed weight, respectively. The effect of B-linked QTLs
on seed oil concentration and 100-seed weight has been also reported in
two high-oil×high-oil mapping populations, GH×PAC2 (Mestries et al. 1998)
and XRQ×PSC8 (Bert et al. 2003). However, the effect of B -linked QTL on
seed oil concentration showed different direction in different genetic
backgrounds.
The seed oil of standard cultivated sunflower is composed primarily of
the saturated fatty acids palmitic (C16:0) and stearic (C18:0), and the
unsaturated oleic (C18:1) and linoleic acids (C18 : 2), with C18:1 and C18:2
accounting for about 90% of the total oil fatty acids (Dorrell and Vick 1997).
The quality of standard sunflower oil is defined by the relative content of
C18:2, which is high in most of the crop grown throughout the world. The
genetic control of the synthesis of stearic acid (C18:0) and oleic acid (C18:1)
in the seed oil of sunflower was studied through candidate-gene and QTL
analysis (Pérez-Vich et al. 2002). Two F 2 mapping populations were
developed using the high C18:0 mutant CAS-3 crossed to either HA-89
(standard, high linoleic fatty acid profile), or HAOL-9 (high C18:1 version
of HA-9). The HA-89 × CAS-3 map comprised 154 markers covering 1,808
cM with a mean spacing of 12.0 cM. The HAOL-9×CAS-3 map comprised
134 markers covering 1,642 cM with a mean interval of 12.5 cM between
markers. Two and four QTLs controlling stearic acid content were detected
in HA-89×CAS-3 (LG 1 and 7) and HAOL-9×CAS-3 (LG 1, 3, 8 and 14),
respectively. The two QTLs detected in HA-89×CAS-3 and four QTLs detected
in HAOL-9×CAS-3 for stearic acid content accounted for 79.3%, and 84.4%
of phenotypic variation, respectively ( Table 5-1 ) . One major QTL affecting
the C18:0 concentration (peak LOD 48.5) was identified on LG 1 in the HA-
89×CAS-3 F 2 population, explaining 78.6% of the phenotypic variation in
the C18:0 concentration. The CAS-3 allele at this QTL locus increased the
C18:0 content. In HAOL-9×CAS-3 F 2 population, two major C18:0 QTLs
were detected. The main C18:0 QTL was detected on LG 1 (peak LOD 50.6)
and it explained 81.3% of the phenotypic variance for this trait. A stearoyl-
ACP desaturase locus (SAD17A) was found to cosegregate with this locus
( Es1 ) controlling the high C18:0. A second major C18:0 QTL was located on
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