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Inheritance of high palmitic acid content in the seed oil of sunflower mutant CAS-5

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Abstract

 Sunflower genotypes with increased levels of palmitic acid (C16 : 0) in the seed oil could be useful for food and industrial applications. The objective of the present study was to determine the inheritance of the high C16 : 0 content in the sunflower mutant line CAS-5 (>25% of the total oil fatty acids). This mutant was reciprocally crossed with the lines HA-89 (5.7% C16 : 0) and BSD-2-691 (5.4% C16 : 0), the latter being the parental line from which CAS-5 was isolated. No maternal effect for the C16 : 0 content was observed from the analysis of F1 seeds in any of the crosses. The inheritance study of the C16 : 0 content in F1, F2 and BC1F1 seeds from the crosses of CAS-5 with its parental line BSD-2-691 indicated that the segregation fitted a model of two alleles at one locus with partial dominance for the low content. The analysis of the fatty acid composition in the F2 populations from the crosses with HA-89 revealed a segregation fitting a ratio 19 : 38 : 7 for low (<7.5%), middle (7.5–15%), and high (>25%) C16 : 0 content, respectively. This segregation was explained on the basis of three loci (P1, P2, P3) each having two alleles showing partial dominance for low content. The genotypes with a high C16 : 0 content were homozygous for the recessive allele p1 and for at least one of the other two recessive alleles, p2 or p3. This model was further confirmed with the analysis of the F3 and the BC1F1 generations. It was concluded that both the recessive alleles p2 and p3 were already present in the BSD-2-691 line, the allele p1 being the result of a mutation from P1. This genetic study will facilitate breeding strategies associated with the incorporation of the high C16 : 0 trait into agronomically acceptable sunflower hybrids.

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Received: 30 March 1998 / Accepted: 13 August 1998

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Pérez-Vich, B., Fernández, J., Garcés, R. et al. Inheritance of high palmitic acid content in the seed oil of sunflower mutant CAS-5. Theor Appl Genet 98, 496–501 (1999). https://doi.org/10.1007/s001220051097

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  • DOI: https://doi.org/10.1007/s001220051097

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