Es-2 Locus Research Articles

Developing Midstearic Acid Sunflower Lines from a High Stearic Acid Mutant

Sunflower (Helianthus annuus L.) genotypes with increased stearic acid (C18:0) content in their seed oil may be useful for food and industrial applications. The objective of this study was to isolate and characterize mid‐stearic acid sunflower lines homozygous recessive for single genes from the high stearic acid mutant CAS‐3 (250 g kg−1). Crosses between CAS‐3 (genotype es1es1es2es2), and the inbred line HA 89, with standard low stearic acid levels (50 g kg−1; Es1Es1Es2Es2), were made to obtain F3 families segregating for either the Es1 or Es2 loci. From these families, F3 half‐seeds with putative genotypes es1es1Es2Es2 (188 g kg−1) and Es1Es1es2es2 (90 g kg−1) were selected. F7–lines homozygous for es1 or es2 were developed. These lines were named CAS‐19 (es1es1Es2Es2) and CAS‐20 (Es1Es1es2es2) and showed mid‐stearic acid levels of 168 g kg−1 (CAS‐19) and 83 g kg−1 (CAS‐20). The fatty acid content was evaluated in all generations by gas‐liquid chromatography. The genetic composition of CAS‐19 and CAS‐20 was verified by evaluating progenies from crosses between both mid‐stearic acid lines, and from crosses between the mid‐stearic acid lines and HA 89. The new Es1Es1es2es2 and es1es1Es2Es2 genotypes expressing mid‐stearic acid levels represent a further advance for the development of sunflower lines for specific edible purposes, and constitute a unique source for agronomic and genetic studies on single alleles controlling increased stearic acid content in sunflower.

Inheritance of Medium Stearic Acid Content in the Seed Oil of a Sunflower Mutant CAS‐4

ABSTRACTThe sunflower (Helianthus annuus L.) line CAS‐4 obtained by mutagenesis has an increased stearic acid (C18:0) content in its seed oil (130 g kg−1), which is desired for some food products. The objectives of this study were to determine (i) the inheritance of medium C18:0 content in CAS‐4, (ii) the relationship between CAS‐4 and the high C18:0 mutant CAS‐3, and (iii) if recombinants with higher C18:0 content than CAS‐3 could be obtained. CAS‐4 was reciprocally crossed with its original parental line RDF‐1‐532 (80 g kg−1 C18:0), HA‐89 (standard low 50 g kg−1 C18:0), and CAS‐3 (250 g kg−1 C18:0). The fatty acid content of the F1, F2, BC1F1 to both parents, and F3 seeds was analyzed by gas‐liquid chromatography (GLC). Alleles controlling low C18:0 exhibited partial dominance to those for medium C18:0, and these were partially dominant to those for high C18:0. Segregation patterns fit a two‐loci model for the HA‐89 × CAS‐4 cross and one‐locus model for the RDF‐1‐532 × CAS‐4 and the CAS‐3 × CAS‐4 crosses. We concluded that medium C18:0 content of CAS‐4 was controlled by alleles at the Es1 and Es2 loci previously identified in CAS‐3, or at tightly linked loci. The CAS‐4 alleles at the Es2 locus are those present in CAS‐3 (es2es2), whereas the alleles at the Es1 locus are different from those of CAS‐3 (es1es1) and have been designated es1bes1b The proposed genotype (C18:0 content) of CAS‐4 is es1bes1bes2es2 The continuous distribution observed in the HA‐89 crosses with CAS‐4 indicated that minor genes and environmental effects also are important in the expression of C18:0 content in CAS‐4.

Genetic control of high stearic acid content in the seed oil of the sunflower mutant CAS-3

A sunflower mutant, CAS-3, with about 25% stearic acid (C18:0) in the seed oil was recently isolated after a chemical-mutagen treatment of RDF-1-532 seeds (8% C18:0). To study the inheritance of the high C18:0 content, CAS-3 was reciprocally crossed to RDF-1-532 and HA-89 (5% C18:0). Significant reciprocal-cross differences were found in one of the two crosses, indicating possible maternal effects. In the CAS-3 and RDF-1-532 crosses, the segregation patterns of the F(1), BC(1), and F(2) populations fitted a one-locus (designated Es1) model with two alleles (Es1, es1) and with partial dominance of low over high C18:0 content. Segregation patterns in the CAS-3 and HA-89 crosses indicated the presence of a second independent locus (designated Es2) with two alleles (Es2, es2), also with partial dominance of low over high C18:0 content. From these results, the proposed genotypes (C18:0 content) of each parent were as follows: CAS-3 (25.0% C18:0) =es1es1es2es2; RDF-1-532 (8.0% C18:0) =Es1Es1es2es2; and HA-89 (4.6% C18:0) =Es1Es1Es2Es2. The relationship between the proposed genotypes and their C18:0 content indicates that the Es1 locus has a greater effect on the C18:0 content than the Es2 locus. Apparently, the mutagenic treatment caused a mutation of Es1 to es1 in RDF-1-532.

Tissue-Specific Expression, Developmental Regulation, and Chromosomal Mapping of the Lecithin: Cholesterol Acyltransferase Gene: Evidence for Expression in Brain and Testes as Well as Liver

Lecithin:cholesterol acyltransferase (LCAT) catalyzes the esterification of cholesterol in high density lipoproteins, thereby facilitating transport of excess cholesterol from peripheral tissues to liver. We report here studies of the developmental, dietary, and genetic control of LCAT gene expression. In adult male Sprague-Dawley rats fed a standard chow diet LCAT mRNA was most abundant in liver, a major source of the plasma enzyme, but appreciable levels were also present in brain and testes. Since both brain and testes are isolated from blood by tight cellular barriers, undoubtedly greatly reducing the level of plasma-derived LCAT in cerebrospinal fluid and testes, the production of LCAT in these tissues may be important for removal of excess cholesterol. Noteworthy changes in the expression of LCAT mRNA were observed during development of both rodents and humans. On the other hand, LCAT mRNA levels were relatively resistant to dietary challenge or to drugs affecting cholesterol metabolism. Since human epidemiological studies have suggested an association between LCAT levels and variations of high density lipoprotein cholesterol, we examined LCAT gene polymorphisms in a mouse animal model. Mapping of the LCAT gene (Lcat) to mouse Chromosome 8 within 2 centimorgans of the Es-2 locus indicates that it does not correspond to any previously mapped loci affecting high density lipoprotein phenotypes in the mouse.

Enzyme polymorphism in the European starling: Study on plasma esterases

In plasma of the European starling ( Sturnus v. vulgaris L.), genetic variation was detected by polyacrylamide gel electrophoresis. Two esterase zones, of which one is polymorphic, had already been described earlier. In addition to these two zones (Es-1 and Es-3), we describe a third (Es-2) that also showed variations. The distribution of the phenotypes observed in the Es-2 zone closely fits the expected distribution according to the law of random mating so that the polymorphism of Es-2 is hereditary. This Es-2 locus is postulated to be a codominant system, controlled by two alleles.

Evidence for separate gene loci (Es-1 and Es-Si) controlling serum esterases in rats.

The presence or absence of the Es-Si esterase (female specific sex-influenced esterase) in rat sera was reexamined by the zymogram technique using agarosegel electrophoresis. It was found that female rat sera of the BN/Kyo strain, which has been typed as the Es-Si esterase negative, display an esterase migrating between the Es-1A esterase and the Es-2C esterase. Using a specific alloantibody to the esterase, it was shown that this esterase is identical to the Es-Si esterase. Thus, BN rats are the first described inbred rats possessing the Es-Si esterase, as well as the Es-1A esterase. Mating experiments between BN rats and SHR rats confirmed a previous demonstration that the presence or absence of the Es-Si esterase is controlled by a single gene locus closely linked to the Es-2 locus where the Es-1 locus also is linked. A further survey with 39 strains by the present methods revealed that besides two sublines of the BN strain, E3/Han, LOU/Max and PVG/Max strains also possess both the ES-1A esterase and the Es-Si esterase. The results indicate that these esterases are controlled by separate gene loci.

Associations of enzymic and chromosomal polymorphisms in the seaweed fly, Coelopa frigida.

Populations of seaweed fly Coelopa frigida are polymorphic at three loci determining the enzymes peptidase-1 (Pep-1), alcohol dehydrogenase (Adh) and larval esterase-2 (Es-2). Alleles at these loci have been shown by others to be non-randomly associated with each other. In the present paper we report non-random associations between the Adh and Es-2 loci and inversions on chromosome I. The two common alleles Adh-B and D are in strong linkage disequilibrium with the alpha and beta inversions, but the Adh-A and C alleles are not so. The X and Y alleles at the Es-2 locus show weak, but still significant, associations with the inversions. We consider possible linkage relationships of the loci on the chromosomal arrangements, and discuss the hypothesis that they constitute part of a coadapted gene complex whose members code for functionally related enzymes.

Serum esterase genetics: identification and hormone induction of the Es-1b esterase in inbred rats.

A previously unrecognized esterase from the sera of the appropriate strains of the rat Rattus norvegicus was revealed by a discontinuous polyacrylamide gel electrophoretic technique. This esterase migrated in the albumin region, whereas a previously known major albumin esterase controlled by the Es-2 locus migrated in the postalbumin region when the method was used. The new albumin esterase component which separated from the Es-2 esterase was identified as the product of the Es-1b gene. The new albumin esterase was not detectable in the sera of sexually mature males of the appropriate genotype, because the activity level of this esterase was influenced by sex hormones, especially androgen.

Genetic study of pancreatic proteinase in mice (Mus musculus): linkage of the Prt-2 locus on chromosome 8.

The Prt-2 locus is linked with Es-1 and Es-2 loci on chromosome 8 (linkage group XVIII). Recombination frequencies were 8.2% between Es-1 and Es-2 12.7% between Es-1 and Prt-2, and 4.5% between Es-2 and Prt-2. From these data, the map position of Prt-2 has been estimated on chromosome 8. The Prt-1 and Prt-3 loci, which are linked very closely on the same chromosome, were not determined.

Linkage of Plasma Esterase Loci in the Chicken

By starch gel electrophoretic method, one of us examined previously the chicken plasma esterases and observed two genetically controlled variations of the esterases. The loci controlling those variations were designated as Es-1 and Es-2. A close linkage relationship of those loci was suggested. This report is concerned with the linkage data involving loci Es-1 and Es-2.The chickens used in this study were Single Comb White Leghorns. Sires (Es-1S/ Es-1S•Es-2A/Es-2A) were mated to dams (Es-1F/Es-1F•Es-2a/Es-2a). F1 progeny thus obtained were crossed to chickens of genotype of Es-1F/Es-1F•Es-2a/Es-2a. The preparation of blood sample, electrophoretic procedure, and staining technique used in this study were identical to those described for the eserine resistant esterases (KIMURA, 1969).The results showed that Es-1 locus was closely linked to Es-2 locus. The rate of crossing over showed a higher value in the male. Recombination frequencies of 0.0358 for the male and 0.0047 for the female were obtained. One of the two possible recombinant types was not detected.

The Effect of Migration on the Maintenance of a Lethal Polymorphism in the House Mouse

Most wild populations of house mice are polymorphic for alleles at the Brachury, T, locus. These alleles are either recessive lethals or viable male steriles and are maintained by an abnormal segregation (transmission) ratio in heterozygous males. The observed frequencies of t alleles in natural populations are considerably less than those expected from deterministic models. This discrepancy has been attributed to the operation of random genetic drift in the small, relatively isolated breeding units (demes) of which a mouse population is comprised. In this investigation, a Monte Carlo simulation of a geographical population has been employed to examine the range of breeding-unit sizes and interdemic migration rates for which the random drift would serve as a likely explanation for the low observed frequencies of the t alleles. In the runs made, lethal t alleles with a transmission ratio of 0.95 were examined. The results of these runs indicate that random drift would only have an important effect on t allele frequencies in populations composed of totally isolated breeding units with a genetically effective size of less than 12 individuals. With 1% migration between demes, the effective breeding-unit size would have to be less than eight. With 3% migration, random drift would only have an important effect on t allele frequencies if the breeding units had a genetically effective size of less than four. Current estimates of these parameters obtained from biochemical polymorphism data (Es-2 locus) indicate that it is quite possible that the breeding-unit sizes and migration rates of natural populations considerably exceed those in which random drift would have an important effect on t allele frequencies. From these considerations it was concluded that random genetic drift itself does not serve as an adequate explanation for the low observed frequencies of lethal t alleles. Brief consideration was given to alternative hypotheses.