Genetic and linkage analysis of cleistogamy in soybean

Early maturing cultivars of soybean [Glycine max (L.) Merr.] native to the shores of the Sea of Okhotsk (Sakhalin and Kuril Islands) and eastern Hokkaido (northern Japan) have been used in breeding for chilling tolerance. These cultivars have a strong tendency to produce cleistogamous flowers throughout their blooming period. This study was conducted to determine the genetic basis of cleistogamy in an early maturing cultivar, Karafuto-1, introduced from Sakhalin. Genetic analysis was performed using F1 plants, the F2 population, and 50 F3 families produced by crossing between Karafuto-1 and a chasmogamous cultivar, Toyosuzu. F2 plants had chasmogamous flowers, indicating that chasmogamy was dominant to cleistogamy. Analysis of F2 populations and F3 families generated segregation data that was close to a two-gene model with epistatic interactions, although a portion of the pooled F3 data on the frequency of chasmogamous segregants from cleistogamous families significantly deviated from the model. The results suggested that a minimum of two genes with epistatic effects were involved in the genetic control of cleistogamy. Furthermore, cleistogamy was associated with early flowering in the F2 and F3 populations. A gene for cleistogamy was linked to one of the recessive genes responsible for insensitivity to incandescent long daylength.     

Genetic analysis and molecular mapping of a pale flower allele at the W4 locus in soybean.

In soybean (Glycine max (L.) Merr.), the w4-mutable line that harbors the w4-m allele was identified in 1983. It was proposed that this line contained an autonomous transposable element at the W4 locus, which is a major locus controlling the biosynthesis of anthocyanin. The w4-m allele can revert to the W4 allele that produces the wild-type phenotype, or sometimes to other alleles that produce intermediate phenotypes. Mutant plants that produce pale flowers were identified among the progeny of a single germinal revertant event from the w4-mutable line. Through genetic analysis, we established that the pale-flower mutation was conditioned by a new allele (w4-p) at the W4 locus. The w4-p allele is dominant to the w4 allele but recessive to the W4 allele, and the w1 allele has an epistatic effect on the w4-p allele. The pale-mutant line (w4-pw4-p) was designated as Genetic Type Collection number T369. An F2 mapping population derived from the cross of Minsoy (W4W4) x T369 (w4-pw4-p) was used to map the W4/w4-p locus, using simple sequence repeat (SSR) markers. The W4 locus was located at one end of molecular linkage group D2, 2.3 cM from the SSR marker Satt386 and close to the nearby telomere.     

Genetic linkage map of the nucleolus organizer region in the soybean

Simple polymorphisms in ribosomal DNA repeats in the nucleolus organizer region (NOR) permitted the development of markers for the genetic mapping of the soybean NOR. The markers map to the top end of soybean linkage group F, one of either telomeric end predicted in the cytogenetic and primary trisomic studies.     

Genetic linkage mapping of the soybean aphid resistance gene in PI 243540

The soybean aphid (Aphis glycines Matsumura) is a pest of soybean [Glycine max (L.) Merr.] in many soybean growing countries of the world, mainly in Asia and North America. A single dominant gene in PI 243540 confers resistance to the soybean aphid. The objectives of this study were to identify simple sequence repeat (SSR) markers closely linked to the gene in PI 243540 and to position the gene on the consensus soybean genetic map. One hundred eighty-four F(2) plants and their F(2:3) families from a cross between the susceptible cultivar Wyandot and PI 243540, and the two parental lines were screened with the Ohio biotype of soybean aphid using greenhouse choice tests. A SSR marker from each 10-cM section of the consensus soybean map was selected for bulked segregant analysis (BSA) to identify the tentative genomic location of the gene. The BSA technique was useful to localize the gene to a genomic region in soybean linkage group (LG) F. The entire F(2) population was then screened with polymorphic SSR markers from this genomic region and a linkage map with nine SSR markers flanking the gene was constructed. The aphid resistance gene was positioned in the interval between SSR markers Satt334 and Sct_033 on LG F. These SSR markers will be useful for marker assisted selection of this gene. The aphid resistance gene from PI 243540 mapped to a different linkage group than the only named soybean aphid resistance gene, Rag1, from 'Dowling'. Also, the responses of the two known biotypes of the soybean aphid to the gene from PI 243540 and Rag1 were different. Thus, the aphid resistance gene from PI 243540 was determined to be a new and independent gene that has been named Rag2.     

Genetic analysis of resistance to soybean mosaic virus in j05 soybean

Soybean cultivar J05 was identified to be resistant to the most virulent strain of soybean mosaic virus (SMV) in northeastern China. However, the reaction of J05 to SMV strains in the United States of America is unknown, and genetic information is needed to utilize this germplasm in a breeding program. The objectives of this study were to determine the reaction of J05 to all US strains of SMV (G1-G7), the inheritance of SMV resistance in J05, and the allelic relationship of resistance genes in J05 with other reported resistance genes. J05 was crossed with susceptible cultivar Essex (rsv) to study the inheritance of SMV resistance. J05 was also crossed with PI 96983 (Rsv1), L29 (Rsv3), and V94-5152 (Rsv4) to test the allelism of resistance genes. F(2) populations and F(2:3) lines from these crosses were inoculated with G1 or G7 in the greenhouse. Inheritance and allelism studies indicate that J05 possesses 2 independent dominant genes for SMV resistance, one at the Rsv1 locus conferring resistance to G1 and necrosis to G7 and the other at the Rsv3 locus conditioning resistance to G7 but susceptibility to G1. The presence of both genes in J05 provides resistance to G1 and G7. J05 is unique from the previous sources that carry 2 genes of Rsv1Rsv3 and will be useful in breeding for SMV resistance.     

Genetic linkage analysis of the carpal tunnel syndrome

Two generations of a family with autosomal dominant carpal tunnel syndrome were studied for genetic linkage to 20 informative polymorphic blood markers. No linkage was demonstrated between the syndrome and the markers tested; exclusion of close linkage (lod score less than -2.0) was found for MNSs, ACP, GALT, GPT, GLO, Hp, Gc, and Pi.     

Genetic linkage analysis of hemoglobin variants in 175 families.

Linkage analysis using the LIPED program developed by Ott for the analysis of whole family data was performed on 175 families with variants of the hemoglobin beta- or gamma-chain. Comparison of our results with those in the literature indicate that there is little evidence for linkage with any of the currently used markers, although there is considerable heterogeneity in lod scores between sexes for the Duffy and MNS blood groups. It is suggested that the most successful approach in the future will be to analyze markers known to be localized on chromosomes which have been indicated as likely sites of the beta-chain locus from hybridization studies.     

Detection and fine-mapping of SC7 resistance genes via linkage and association analysis in soybean

Soybean mosaic virus (SMV) disease is one of the most serious and broadly distributed soybean (Glycine max (L.) Merr.) diseases. Here, we combine the advantages of association and linkage analysis to i...     

Analysis of flavonoids in flower petals of soybean near-isogenic lines for flower and pubescence color genes

W1, W3, W4, and Wm genes control flower color, whereas T and Td genes control pubescence color in soybean. W1, W3, Wm, and T are presumed to encode flavonoid 3'5'-hydroxylase (EC 1.14.13.88), dihydroflavonol 4-reductase (EC 1.1.1.219), flavonol synthase (EC 1.14.11.23), and flavonoid 3'-hydroxylase (EC 1.14.13.21), respectively. The objective of this study was to determine the structure of the primary anthocyanin, flavonol, and dihydroflavonol in flower petals. Primary component of anthocyanin in purple flower cultivars Clark (W1W1 w3w3 W4W4 WmWm TT TdTd) and Harosoy (W1W1 w3w3 W4W4 WmWm tt TdTd) was malvidin 3,5-di-O-glucoside with delphinidin 3,5-di-O-glucoside as a minor compound. Primary flavonol and dihydroflavonol were kaempferol 3-O-gentiobioside and aromadendrin 3-O-glucoside, respectively. Quantitative analysis of near-isogenic lines (NILs) for flower or pubescence color genes, Clark-w1 (white flower), Clark-w4 (near-white flower), Clark-W3w4 (dilute purple flower), Clark-t (gray pubescence), Clark-td (near-gray pubescence), Harosoy-wm (magenta flower), and Harosoy-T (tawny pubescence) was carried out. No anthocyanins were detected in Clark-w1 and Clark-w4, whereas a trace amount was detected in Clark-W3w4. Amount of flavonols and dihydroflavonol in NILs with w1 or w4 were largely similar to the NILs with purple flower suggesting that W1 and W4 affect only anthocyanin biosynthesis. Amount of flavonol glycosides was substantially reduced and dihydroflavonol was increased in Harosoy-wm suggesting that Wm is responsible for the production of flavonol from dihydroflavonol. The recessive wm allele reduces flavonol amount and inhibits co-pigmentation between anthocyanins and flavonols resulting in less bluer (magenta) flower color. Pubescence color genes, T or Td, had no apparent effect on flavonoid biosynthesis in flower petals.     

Genetic linkage analysis of oral lichen planus in a Chinese family

Oral lichen planus (OLP) is a common oral inflammatory disease affecting about 1-2% of the general adult population. As with European families who are diagnosed with OLP, the Chinese family who we studied was diagnosed with a severe form of oral reticular and erosive lesions; moreover, two of the five affected individuals developed oral cancer at an early age. A whole-genome genotyping scan with linkage analysis was performed using the 10K SNP array to investigate the genetic susceptibility of the Chinese family to OLP, which revealed one maximal nonparametric LOD score of 2.32 (P = 0.0156) for SNP marker rs2372736, defined at the chromosome 3p14-3q13 region encompassing 19 SNPs. Blood samples were obtained from 10 members of the family, which included the grandmother, father and mother, and the children altogether. The grandfather is dead, but the family members remembered he also suffered from the same disease. Chromosome 3p14-3q13 was identified as the candidate gene region for OLP; this information provides a foundation for further identification of the gene responsible for OLP.     

Genetic linkage analysis of X-ray hypersensitivity in the LEC mutant rat

The LEC rat has been reported to exhibit X-ray hypersensitivity and deficiency in DNA double-strand break (DSB) repair. The present study was performed to map the locus responsible for this phenotype, the xhs (X-ray hypersensitivity), as the first step in identifying the responsible gene. Analysis of the progeny of (BN × LEC)F₁× LEC backcrosses indicated that the X-ray hypersensitive phenotype was controlled by multiple genetic loci in contrast to the results reported previously. Quantitative trait loci (QTL) linkage analysis revealed two responsible loci located on Chromosomes (Chr) 4 and 1. QTL on Chr 4 exhibited very strong linkage to the X-ray hypersensitive phenotype, while QTL on Chr 1 showed weak linkage. The Rad52 locus, mutation of which results in hypersensitivity to ionizing radiation and impairment of DNA DSB repair in yeast, was reported to be located on the synteneic regions of mouse Chr 6 and human Chr 12. However, mapping of the rat Rad52 locus indicated that it was located 23 cM distal to the QTL on Chr 4. Furthermore, none of the radio-sensitivity-related loci mapped previously in the rat chromosome were identical to the QTL on Chrs 4 and 1 in the LEC rat. Thus, it seems that X-ray hypersensitivity in the LEC rat is caused by mutation(s) in as-yet-undefined genes. Received: 14 February 2000 / Accepted: 17 May 2000     

Genetic regulation of flower development

Flower development provides a model system to study mechanisms that govern pattern formation in plants. Most flowers consist of four organ types that are present in a specific order from the periphery to the centre of the flower. Reviewed here are studies on flower development in two model species:Arabidopsis thaliana andAntirrhinum majus that focus on the molecular genetic analysis of homeotic mutations affecting pattern formation in the flower. Based on these studies a model was proposed that explains how three classes of regulatory genes can together control the development of the correct pattern of organs in the flower. The universality of the basic tenets of the model is apparent from the analysis of the homologues of theArabidopsis genes from other plant species     

Genetic control of flower development

Flowering plants are the most highly evolved and complex organisms within the plant kingdom. The flower consists of several distinct organ systems that are responsible for higher plant reproduction. Cells within specific floral organs differentiate into spores and gametes required by the plant to complete its life cycle. Flower development represents an excellent model for understanding the molecular and physiological processes that control organ differentiation in higher plants. Rapidly emerging gene tagging procedures are facilitating the isolation of genes that control flower morphogenesis.     

Genetic and linkage analysis of familial congenital hypothyroidism: exclusion of linkage to the TSH receptor gene

Congenital hypothyroidism affects 1/3000– 4000 newborns. The causes of this group of disorders are still largely unknown. Although most cases are sporadic, some families have several affected children and/or consanguineous parents, suggesting autosomal recessive inheritance. Furthermore, there is a murine strain (hyt) with congenital hypothyroidism and autosomal recessive inheritance, whose phenotype appears to be identical with the corresponding human disease. In the hyt mouse, the disease is caused by a mutation in the thyroid-stimulating hormone receptor (TSHR) gene, making this gene a likely candidate also for the human disease. The human TSHR gene was mapped on radiation hybrid panels and closely linked flanking markers D14S287 and D14S616 were identified. On the Genebridge 4 panel, D14S287 was found to be located 8.5 cR (corresponding to 2.3 cM) proximal to the TSHR gene, and D14S616 was found to be located 4.4 cR (1.2 cM) distal to the TSHR gene. These markers were analyzed in 23 families, most of them with two or more children affected by congenital hypothyroidism and some with appreciable consanguinity of the parents. Assuming homogeneity, the two-point lod score at θ = 0.1 was –4.8 for D14S287 and –5.8 for D14S616, and thus linkage to the TSHR gene was excluded. Even when the data were analyzed with allowance for heterogeneity, there was no evidence of linkage. Our conclusion is that if mutation of the TSHR gene causes familial congenital hypothyroidism in humans, it affects only a small proportion of the cases. Received: 8 July 1996     

Genetic hemochromatosis and HLA linkage

Summary We previously reported five families with primary, genetic (idiopathic) hemochromatosis in whom HLA typing of subjects indicated that a homozygous-heterozygous mating had almost certainly occurred and in whom inheritance of the disease trait was best explained by an autosomal recessive mode of inheritance. However, in one family, two children apparently homozygous for hemochromatosis did not manifest overt evidence of the disease, and alternative explanations were postulated, including autosomal dominant inheritance in this family. Subsequent study of the family members, including repeat HLA-DR serology with more recently defined antisera and DNA genotyping at the HLA-DR locus has, we believe, provided the true explanation for the previous apparent anomaly and adds further evidence for the tight linkage of the disease to the HLA-A locus.