Charecteristic of stearic acid for topical application
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Stearic Acid (18:0)
Stearic acid in a typical soybean cultivar comprises ∼4% of the seed oil, though considerable variation exists, with ranges reported between ∼3% and >35% (Fehr, 2007). Although stearic acid is a fully saturated fatty acid, it does not appear to result in increased levels of LDL cholesterol in serum, in contrast to the noted elevation of LDL cholesterol due to dietary intake of palmitic acid (Yu et al., 1995). No alleles have been reported which result in substantial reduction of stearic acid content below about 3% of total oil, though minor genes may play a role in the variation noted resulting from certain genetic crosses (Fehr, 2007). As a result, breeding for reduced saturate content of soybean seed oil has largely focused on identification and introgression of alleles responsible for reduced palmitic acid content.
Increasing the level of stearic acid in soybean oil has been promoted as a means to improve oil stability, as well as to improve utility for baking applications. Mutant alleles that result in elevated levels of
stearic acid in the seed are referred to as either fas or st (Pantalone et al., 2004). The first reported elevated stearic acid mutant allele was the fas1 -a allele from sodium azide-induced mutant line FA8077/A6 (Hammond & Fehr, 1983). Three independent allelic mutant alleles of the fas1 locus have been identified, with slightly different stearic content: fas from A81-606085 (19%
stearic acid), fasa from A6 (30%
stearic acid), and fasb from line FA41545 (15% stearic acid). Another naturally occurring fas1 mutation, fas1-nc , is allelic to
fas1-a . Recently, the mutational basis behind the most pronounced elevated stearic acid phenotype in line A6 ( fas1-a ) has been determined to be due to a deletion of a seed specific δ9–Stearoyl-ACP-Desaturase ( SACPD-C ) gene (Zhang et al., 2008). Several additional independent mutations, all of which are allelic to fas1-a, have also been developed by EMS mutagenesis (recently reviewed in Fehr, 2007).
Two other sources of elevated stearic acid mutant alleles have been determined: KK-2 and M25, which possess the non-allelic st and st genes, respectively. Genetic analysis of the progeny of a cross between these lines revealed that the combination of these two independent mutant loci results in
stearic acid levels greater than 35% of the seed oil (Rahman et al., 1997). It is not currently clear whether the st or st loci are allelic to fas1 , nor has the underlying genetic basis for the stearic acid elevation from these lines been reported in the literature.
It has also been suggested that modifier genes may play significant roles when crosses with the three sources of fas1 alleles do not result in stearic acid phenotypes identical to the parents (Lundeen et al., 1987). Whether such results have a genetic basis or are simply attributed to experimental error has not been determined.
Stearic acid in a typical soybean cultivar comprises ∼4% of the seed oil, though considerable variation exists, with ranges reported between ∼3% and >35% (Fehr, 2007). Although stearic acid is a fully saturated fatty acid, it does not appear to result in increased levels of LDL cholesterol in serum, in contrast to the noted elevation of LDL cholesterol due to dietary intake of palmitic acid (Yu et al., 1995). No alleles have been reported which result in substantial reduction of stearic acid content below about 3% of total oil, though minor genes may play a role in the variation noted resulting from certain genetic crosses (Fehr, 2007). As a result, breeding for reduced saturate content of soybean seed oil has largely focused on identification and introgression of alleles responsible for reduced palmitic acid content.
Increasing the level of stearic acid in soybean oil has been promoted as a means to improve oil stability, as well as to improve utility for baking applications. Mutant alleles that result in elevated levels of
stearic acid in the seed are referred to as either fas or st (Pantalone et al., 2004). The first reported elevated stearic acid mutant allele was the fas1 -a allele from sodium azide-induced mutant line FA8077/A6 (Hammond & Fehr, 1983). Three independent allelic mutant alleles of the fas1 locus have been identified, with slightly different stearic content: fas from A81-606085 (19%
stearic acid), fasa from A6 (30%
stearic acid), and fasb from line FA41545 (15% stearic acid). Another naturally occurring fas1 mutation, fas1-nc , is allelic to
fas1-a . Recently, the mutational basis behind the most pronounced elevated stearic acid phenotype in line A6 ( fas1-a ) has been determined to be due to a deletion of a seed specific δ9–Stearoyl-ACP-Desaturase ( SACPD-C ) gene (Zhang et al., 2008). Several additional independent mutations, all of which are allelic to fas1-a, have also been developed by EMS mutagenesis (recently reviewed in Fehr, 2007).
Two other sources of elevated stearic acid mutant alleles have been determined: KK-2 and M25, which possess the non-allelic st and st genes, respectively. Genetic analysis of the progeny of a cross between these lines revealed that the combination of these two independent mutant loci results in
stearic acid levels greater than 35% of the seed oil (Rahman et al., 1997). It is not currently clear whether the st or st loci are allelic to fas1 , nor has the underlying genetic basis for the stearic acid elevation from these lines been reported in the literature.
It has also been suggested that modifier genes may play significant roles when crosses with the three sources of fas1 alleles do not result in stearic acid phenotypes identical to the parents (Lundeen et al., 1987). Whether such results have a genetic basis or are simply attributed to experimental error has not been determined.
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