Biology Reference
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variation (Vear et al. 1997a). Also, different genotypes appear to possess
resistances to different phases of the disease cycle (Viguié et al. 2000).
Bert et al. (2002) identified the QTLs controlling resistance to mycelium
extension on leaves. They placed a mycelial explant on the upper side of the
leaf tip and tested the rate of lesion development from this explant. An F 2
mapping population from the cross XRQ×PSC8 was used for this study and
the experiment was conducted in three years 1998, 1999 and 2000. Two,
three and three QTLs were identified for mycelium extension rate respectively
in 1998 (LG 4 and 10 with total R 2 of 27.7%), 1999 (LG 4, 8 and 14 with total
R 2 of 59.3%) and 2000 (LG 4, 8 and 17 with total R 2 of 47.2%). For the mean of
three years, four QTLs were identified on LG 4, 8, 10 and 17 with total
phenotypic variance explained of 49.2%. Results showed that both the
parental lines transmitted the positive alleles for the QTLs. Interestingly the
linkage groups 4, 8 and 10 contained QTLs for resistance to mycelium
extension on leaves detected in 1998, 1999 and 2000 that showed a partially
stable QTLs across years.
5.2.2.3 Resistance to Phoma macdonaldii
Black stem, caused by Phoma macdonaldii , is one of the most important diseases
of sunflower in the world. It causes premature ripening associated with
yield losses of 10-30%, and also reduction in oil content and 1,000-seed
weight (Carson 1991). Roustaee et al. (2000), using parental genotypes and
their F 1 hybrids, showed that the variation among genotypes studied was
due to general combining ability and thus most of the variation was
attributed to additive effects. Developing partially resistant genotypes using
QTL approach is the main challenge to cope with this disease.
Rachid Al-Chaarani et al. (2002) identified seven QTLs for resistance to
black stem using an AFLP-based RIL map of the cross PAC2×RHA266
( Table 5-1 ) . A population of 83 RILs was used for inoculation with an
agressive monopycniospore isolate of P. macdonaldii produced from naturally
infected plants in the south-west of France. The seven detected QTLs for
black stem resistance jointly explained 92% of the total phenotypic variance
and were located on LG 3, 4, 8, 9, 11, 15 and 17. For six of the seven QTLs, the
parent RHA266 conferred positive alleles and the parent PAC2 contributed
to positive alleles in only one QTL.
In a later study, Bert et al. (2004) used a population of 150 F 2 :F 3 plants
from the cross between FU (an unbranched maintainer line) and PAZ2 (a
male fertility restorer line) for mapping QTLs involved in resistance to P.
macdonaldii ( Table 5-1 ) . A genetic linkage map of 18 LGs (a pseudo LG) with
216 molecular markers spanning 1,937 cM was constructed. Four QTLs
were identified for resistance to P. macdonaldii necrosis on LGs 1, 3, 15 and
16, which explained all together 39% of the phenotypic variance. The LOD
 
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