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Dominant Alleles (dominant + allele)
Selected AbstractsThe Characterization and Geographical Distribution of the Genes Responsible for Vernalization Requirement in Chinese Bread WheatJOURNAL OF INTEGRATIVE PLANT BIOLOGY, Issue 4 2009Qing-Ming Sun Abstract The frequency and distribution of the major vernalization requirement genes and their effects on growth habits were studied. Of the 551 bread wheat genotypes tested, seven allelic combinations of the three Vrn-1 genes were found to be responsible for the spring habit, three for the facultative habit and one for the winter habit. The three Vrn-1 genes behaved additively with the dominant allele of Vrn-A1 exerting the strongest effect. The allele combinations of the facultative genotypes and the discovery of spring genotypes with "winter" allele of Vrn-1 implied the presence of as yet unidentified alleles/genes for vernalization response. The dominant alleles of the three Vrn-1 genes were found in all ten ecological regions where wheat is cultivated in China, with Vrn-D1 as the most common allele in nine and Vrn-A1 in one. The combination of vrn-A1vrn-B1Vrn-D1 was the predominant genotype in seven of the regions. Compared with landraces, improved varieties contain a higher proportion of the spring type. This was attributed by a higher frequency of the dominant Vrn-A1 and Vrn-B1 alleles in the latter. Correlations between Vrn-1 allelic constitutions and heading date, spike length, plant type as well as cold tolerance were established. [source] Identification of a single dominant allele for resistance to blackleg in Brassica napus,Surpass 400'PLANT BREEDING, Issue 6 2003C.-X. Li Abstract The inheritance of resistance to blackleg (caused by Leptosphaeria maculans) was examined in the F1 and F2 of a cross between highly resistant canola ,Surpass 400' and susceptible ,Westar' in the field. Blackleg-infected canola straw was collected from the field and scattered among plants to increase disease development with the aid of natural rainfall. Disease severity on seedlings was assessed as the average number of lesions on leaves 1 and 2, and on adult plants as the percentage necrosis on a cross-section of stems immediately above the crown. All ,Westar' plants were susceptible (S) and all ,Surpass 400' and F1 plants were resistant (R) at both growth stages. Disease severity on F2 plants segregated 3 : 1 (R : S) as expected for a single dominant resistance allele in both the seedling and adult plant stages. There was a high proportion (91.1%) of matching reactions (R-R and S-S) between seedling and adult plants. ,Surpass 400' is the source of a single dominant allele for blackleg resistance in Brassica napus that is expressed strongly in both seedlings and adult plants. [source] Neonatal salt-wasting and 11 ,-hydroxylase deficiency in a child carrying a homozygous deletion hybrid CYP11B2 (aldosterone synthase),CYP11B1 (11 ,-hydroxylase)CLINICAL GENETICS, Issue 3 2004B Ezquieta This article reports the case of a boy diagnosed at 1.8 years of age with congenital adrenal hyperplasia due to 11 ,-hydroxylase deficiency. The patient showed salt-wasting episodes during the neonatal period. On molecular analysis, a homozygous deletion hybrid (CYP11B2,CYP11B1) involving the CYP11B locus at 8q24.3 was found. Southern blot analysis showed the break point of the chimera gene to be located before intron 5; sequence analysis identified it at exon 4 between codons 202 and 248. This CYP11B2(5,)/B1(3,) hybrid should lack aldosterone synthase activity (due to the CYP11B1 residues at exons 5 and 6), and the enzyme it codes for should not be promoted by adrenocorticotropic hormone (ACTH) (CYP11B2 promoter sequences). The patient phenotype , neonatal salt-wasting and 11 ,-hydroxylase deficiency , is in agreement with this hybrid structure. This is the first time a homozygous deletion hybrid generated by unequal crossover has been described in exon 4. This genetic lesion appears to be the reciprocal product from the recombination event that causes glucocorticoid-remediable aldosteronism, a duplication dominant allele (CYP11B2,CYP11B1/B2,CYP11B1) coding for additional aldosterone synthase activity regulated by ACTH. The clinical presentation of the condition in this patient contributes to the in vivo understanding of the regulation of this complex locus in which two ,duplicated' genes have evolved different regulatory and enzymatic activities involved in mineralocorticoid and glucocorticoid synthesis in the adrenal glands. The fact that this allele was first predicted and has now been documented clinically and molecularly in vivo is particularly noteworthy. [source] EFFECTS OF GENETIC DRIFT ON VARIANCE COMPONENTS UNDER A GENERAL MODEL OF EPISTASISEVOLUTION, Issue 10 2004N.H. Barton Abstract We analyze the changes in the mean and variance components of a quantitative trait caused by changes in allele frequencies, concentrating on the effects of genetic drift. We use a general representation of epistasis and dominance that allows an arbitrary relation between genotype and phenotype for any number of diallelic loci. We assume initial and final Hardy-Weinberg and linkage equilibrium in our analyses of drift-induced changes. Random drift generates transient linkage disequilibria that cause correlations between allele frequency fluctuations at different loci. However, we show that these have negligible effects, at least for interactions among small numbers of loci. Our analyses are based on diffusion approximations that summarize the effects of drift in terms of F, the inbreeding coefficient, interpreted as the expected proportional decrease in heterozygosity at each locus. For haploids, the variance of the trait mean after a population bottleneck is var(,z,) =where n is the number of loci contributing to the trait variance, VA(1)=VA is the additive genetic variance, and VA(k) is the kth-order additive epistatic variance. The expected additive genetic variance after the bottleneck, denoted (V*A), is closely related to var(,z,); (V*A) (1 ,F)Thus, epistasis inflates the expected additive variance above VA(1 ,F), the expectation under additivity. For haploids (and diploids without dominance), the expected value of every variance component is inflated by the existence of higher order interactions (e.g., third-order epistasis inflates (V*AA)). This is not true in general with diploidy, because dominance alone can reduce (V*A) below VA(1 ,F) (e.g., when dominant alleles are rare). Without dominance, diploidy produces simple expressions: var(,z,)==1 (2F) kVA(k) and (V*A) = (1 ,F)k(2F)k-1VA(k) With dominance (and even without epistasis), var(,z,)and (V*A) no longer depend solely on the variance components in the base population. For small F, the expected additive variance simplifies to (V*A)(1 ,F) VA+ 4FVAA+2FVD+2FCAD, where CAD is a sum of two terms describing covariances between additive effects and dominance and additive × dominance interactions. Whether population bottlenecks lead to expected increases in additive variance depends primarily on the ratio of nonadditive to additive genetic variance in the base population, but dominance precludes simple predictions based solely on variance components. We illustrate these results using a model in which genotypic values are drawn at random, allowing extreme and erratic epistatic interactions. Although our analyses clarify the conditions under which drift is expected to increase VA, we question the evolutionary importance of such increases. [source] A quantitative genetic study of cephalometric variables in twinsORTHODONTICS & CRANIOFACIAL RESEARCH, Issue 3 2001C. Carels This study aimed at determining the relative genetic and environmental impact on a number of well-known cephalometric variables in twins. In order to find a clue in the heritability pattern of some dentofacial characteristics and on the expected limits of the therapeutic impact on the dentofacial subparts they are representing. Cephalograms were collected from 33 monozygotic and 46 dizygotic twins, who did not undergo any orthodontic treatment. Nineteen linear and four angular variables were selected all representing a different definite subpart of the dentofacial complex. The reproducibility of the measurement of most of the linear variables was very high. A genetic analysis using model fitting and path analysis was carried out. First, data were checked on the fulfilment of the conditions for genetic analysis in twins reared together. The results show that the genetic determination is significantly higher for vertical (72%) than for horizontal (61%) variables. As far as the genetic component is concerned, all variables selected seem to be inherited by additive genes, except for mandibular body length, which was determined by dominant alleles. Sex differences in genetic determination were found for the anterior face height, showing a significantly higher genetic component for boys (91%) than for girls (68%). For the angular measurements, no genetic influence was found: only environmental influences common to both members of each pair could be demonstrated. [source] Inheritance of resistance to broomrape (Orobanche cumana Wallr.) race F in a sunflower line derived from wild sunflower speciesPLANT BREEDING, Issue 1 2007L. Velasco Abstract Genetic resistance to broomrape (Orobanche cumana Wallr.) race F in sunflower line J1, derived from the wild perennial species Helianthusgrosseserratus Martens and Helianthus divaricatus L., has been reported to be controlled by dominant alleles at a single locus, Or6. However, deviations from this monogenic inheritance have been observed. The objective of the present study was to gain insight into the inheritance of resistance to broomrape race F in the sunflower line J1. F1, F2, F3 and BC generations from crosses between J1 and three susceptible lines, P21, NR5 and HA821 were evaluated. F1 hybrids showed both resistant (R) and moderately resistant (MR) plants, the latter having a maximum of five broomrape stalks per plant compared with >10 in the susceptible parents. This indicated incomplete dominance of the Or6 alleles. F2 plants were classified as R, MR or susceptible (more than five broomrape stalks per plant). Three different segregation ratios were observed: 3 : 1, 13 : 3 and 15 : 1 (R + MR : S), suggesting the presence of a second gene, Or7, whose expression was influenced by the environment. A digenic model was confirmed, based on the evaluation of F2:3 families. [source] Inheritance of heading time in spring barley evaluated in multiple environmentsPLANT BREEDING, Issue 3 2001L. W. Gallagher Abstract The inheritance of heading time of spring barley was studied in three extremely early genotypes IB, RL and ,Mona' (M), which is homozygous recessive for the early maturity ea8 (=eak) gene conferring extreme earliness under short daylengths and is relatively photoperiod insensitive, and five (GP, MA, PS, NU and BA) spring genotypes that are early to intermediate for heading time. Frequency distributions of F2 generations grown at Ouled Gnaou, Morocco (32°15, N), an environment which maximizes differences between photoperiod-insensitive and photoperiod-sensitive genotypes, indicated that across populations many loci were segregating in a complex Mendelian manner. IB and RL were both homozygous recessive for the ea8 gene, which conferred an early heading time. RL had partially dominant alleles at second locus (Enea8), which enhanced its earliness. Recovery of only progeny within the parental range of genotypes for heading time from the crosses of RL/M and IB/M suggests that numerous loci remained suppressed, perhaps latent, given their diverse parentage. The ea8 recessive homozygote in RL suppressed another unidentified locus which, when homozygous recessive in the absence of the ea8 recessive homozygote, conferred extreme earliness in one short daylength environment (Ouled Gnaou, Morocco) but was undetected in another environment (Davis, CA, USA). Epistatic gene action and genotype × environment effects strongly influenced heading time. In addition to a genetic system consisting of single-locus recessive homozygotes conferring photoperiod insensitivity, a second genetic system, based on dominant alleles at one or a few loci, derived from the early heading Finnish landrace ,Olli', also confers extremely early heading time under short daylengths and relative photoperiod insensitivity in the genotype GP. [source] Grey plumage colouration in the duck is genetically determined by the alleles on two different, interacting lociANIMAL GENETICS, Issue 1 2010Y. Gong Summary Based on the observation of a grey phenotype in the F1 generation from a cross between two white plumage duck varieties, the white Kaiya and the white Liancheng, we hypothesized a possible interaction between two autosomal loci that determine grey plumage. Using the parental and F1 individuals, seven testing combinations including five different F1 intercrosses (F2) and two different backcrosses (BC1 and BC2) were designed to test our hypothesis. It was demonstrated by chi-squared analysis that six test matings produced offspring in the expected ratios between the grey and white, with P- values ranging from 0.50 to 0.99. Another mating, where all white offspring were expected, produced 33 white individuals. These results verified that the interaction between two loci produced the grey phenotype. The C locus, which carries the recessive allele (c), was previously thought to be the only gene responsible for white plumage in the duck. This is the first report that an allele (t), carried by the white Liancheng at a different autosomal locus, also determines white plumage in ducks. Furthermore, the dominant alleles at both loci can interact with each other to produce the grey phenotype, and a new dark phenotype, observed in some F2 individuals, can be attributed to the dosage effect of the T allele. [source] |