Gene Cloning and Characterization - Genetics, Genomics and Breeding of Crop Plants - page 208

Osorio et al. (1995) induced additional variability in the fatty acid pattern
for sunflower by mutagenesis using ethylmethane sulfonate, sodium azide
and X-rays. Four sunflower mutants with altered seed fatty acids
composition were isolated: CAS-5, which has oil with a five-fold increase in
palmitic acid (C16:0). CAS-3, CAS-4, and CAS-8 have two- to six-fold stearic
acid (C18:0) content compared to the normal content observed in the oil of
cultivated sunflower. Osorio et al. (1995) concluded that according to the
bimodal distribution in fatty acid composition of CAS-3 and CAS-5 major
recessive genes were involved in the control of these traits.
Pérez-Vich et al. (1999) studied the inheritance and the genetic control
of the CAS-3 mutants in detail. They found that inheritance of the C18:0
content in F 1 , F 2 , and BC 1 F 1 seeds from the cross of CAS-3 with their parental
lines indicated the presence of partially recessive alleles at two independent
loci Es 1 and Es 2 controlling the high stearic acid content in the seed oil of
this mutant. Candidate gene and quantitative trait loci (QTL) analyses
demonstrated that Es 1 cosegregates with a stearoyl-acyl carrier protein (ACP)
desaturase locus ( SAD17A ) and underlies the major QTL affecting the
concentration of stearic acid in CAS-3. This QTL has been named st1-SAD17A
and is located on LG 1 of the sunflower genetic map (Pérez-Vich et al. 2002).
Later on, Pérez-Vich et al. (2004) mapped three minor QTLs for increased
stearic acid content in sunflower seed oil on LG 3, LG 11, and LG 13 of the
sunflower genetic map (Tang et al. 2002).
Pérez-Vich et al. (2005, 2006a) also reported mapping of the very high
stearic acid gene Es 3 from a mutant CAS-14 and identified PCR-based
molecular markers linked to this gene. Genetic characterization of the CAS-
14 mutant (Pérez-Vich et al. 2006b) showed that the very high stearic acid
content in this line, which shows a gradient within the seed from embryo to
distal extreme of the seed, is controlled by a single recessive gene ( es 3),
segregating independently of the Es 1 gene with a major effect on stearic acid
content in CAS-3. In addition, the mutation in the Es3 gene did not coincide
with any boundary group associated to stearoyl-acyl carrier protein
desaturase (SAD) enzymes (Pérez-Vich et al. 2005). However, expression
analyses of SAD6 and SAD17 , two genes coding for SAD forms expressed at
high level in sunflower seeds during oil synthesis, showed a coordinated
decrease in transcription corresponding to the decrease in enzyme activity
(Salas et al. 2008). The observed downregulation of both genes in CAS-14
demonstrated as the previous genetic studies that CAS-3 and CAS-14
represent distinct different mutations. As the mutation did not map within
the boundary groups corresponding to SAD genes this means that an
alteration in a trans- regulatory element affected the expression of these
desaturases. Therefore, the gene responsible for the CAS-14 phenotype
probably encodes a transcription factor that regulates the expression of
SAD6 and SAD17 (Salas et al. 2008). Pérez-Vich et al. (2006b) mapped the