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21.
Chloroplast and mitochondrial DNA are paternally inherited in Sequoia sempervirens D. Don Endl 总被引:7,自引:2,他引:5
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Neale DB Marshall KA Sederoff RR 《Proceedings of the National Academy of Sciences of the United States of America》1989,86(23):9347-9349
Restriction fragment length polymorphisms in controlled crosses were used to infer the mode of inheritance of chloroplast DNA and mitochondrial DNA in coast redwood (Sequoia sempervirens D. Don Endl.). Chloroplast DNA was paternally inherited, as is true for all other conifers studied thus far. Surprisingly, a restriction fragment length polymorphism detected by a mitochondrial probe was paternally inherited as well. This polymorphism could not be detected in hybridizations with chloroplast probes covering the entire chloroplast genome, thus providing evidence that the mitochondrial probe had not hybridized to chloroplast DNA on the blot. We conclude that mitochondrial DNA is paternally inherited in coast redwood. To our knowledge, paternal inheritance of mitochondrial DNA in sexual crosses of a multicellular eukaryotic organism has not been previously reported. 相似文献
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Given that knowledge regarding the etiology of comorbidity between disorders can have a significant impact on research regarding the classification, treatment, and etiology of the disorders, the ability to reject incorrect hypotheses regarding the causes of comorbidity is very important. A simulation study was conducted to assess the validity of the Neale and Kendler (1995) model-fitting approach in examining the etiology of comorbidity between two disorders. First, data were simulated under the assumptions of the 13 alternative comorbidity models described by Neale and Kendler. Second, model-fitting analyses testing the comorbidity models were conducted on the simulated datasets. Thirteen sets of data with varying model parameters were simulated to test Neale and Kendler's assertion that their model-fitting approach is appropriate across a range of potential prevalences and degrees of familiality. The validity of the model-fitting approach in examining unselected twin data and a combination of selected family data and unselected family data was explored. The model-fitting approach successfully discriminated several classes of comorbidity models, although discrimination between models within classes of related models was less accurate. Results suggest that the model-fitting approach can be a useful tool in examining the etiology of the comorbidity between disorders if the caveats of the present study's results are considered carefully. As predicted by Neale and Kendler, variations in the disorder prevalences and familial correlations did not affect the validity of their model-fitting approach, but affected the power to discriminate the correct model. As suggested by Neale and Kendler, the model-fitting approach can be applied to both unselected and selected data and to both twin and family data. 相似文献
24.
25.
Progress in the autosomal segmental aneusomy syndromes (SASs): single or multi-locus disorders? 总被引:3,自引:2,他引:3
Based on cytogenetic observations, several syndromes have been previously
identified as microdeletion-based disorders. In this review, recent
progress is presented regarding whether one or multiple genes can be
implicated in the pathogenesis of these segmentally aneusomic syndromes.
The syndromes discussed include Angelman, Alagille, Williams,
Langer-Giedeon, Prader-Willi, Smith-Magenis, Miller-Dieker, and
DiGeorge/velocardiofacial or the 22q11 deletion syndromes. For Angelman and
Alagille syndromes, single genes have been identified, whereas for Williams
and Langer-Giedion syndromes, more than one gene can be implicated.
Although there has been significant progress in dissecting the molecular
basis for the other disorders, the ultimate answer regarding one versus
several genes remains to be determined.
相似文献
26.
Kenneth S. Kendler Ellen E. Walters Kim R. Truett Andrew C. Heath Michael C. Neale Nicholas G. Martin Lindon J. Eaves 《Behavior genetics》1995,25(6):499-515
Self-report symptoms of anxiety are widely used in mental health and social science research as an index of current psychiatric
state. Previous twin studies have suggested that genetic factors account for a significant proportion of the variance in these
symptoms. To replicate and extend these findings, we examined self-report symtoms of panic-phobia and somatization in the
“Virginia 30,000” twin-family sample. Model fitting applied to 80 unique relationships in the twin-family pedigree produced
the following major results: (i) genetic effects were significant for both symptom factors, accounting for between 25 and
49% of the total variance, with the exception of symptoms of panic-phobia in females, where they accounted for 15–16% of the
variance; (ii) familial environmental effects were absent for symptoms of somatization, while for symptoms of panic-phobia
they accounted for a very small proportion of variance in males (≤1.2%) and a modest proportion in females (6–17%) (iii) spousal
correlations were present for both factors, ranging from +0.05 to +0.20; (iv) genetic factors which influenced symptoms were
generally the same in males and females, although their effect was greater in males; (v) heritability estimates were lower
in the population-based than in the volunteer sample; and (vi) when test-retest reliability was included in the model, results
suggest that genetic factors account for at least half of the stable variance for all symptom factors, except panic-phobia
in females. Our results support the validity of previous twin studies of self-report symptoms of anxiety and suggest that
genetic factors significantly influence these symptoms but familial-environmental factors play little or no etiologic role. 相似文献
27.
Rabbits immunized with autologous renal tubular antigen (Fx1A) developed tubulointerstitial nephritis whereas sheep anti-Fx1A antibody administered i.v. produced glomerulonephritis (GN). This lesion showed heavy granular glomerular deposition of immunoglobulin and subepithelial electron dense deposits, early proteinuria, leucocyte independence and a temporal pattern of quantitated glomerular antibody binding distinct from that reported to occur in passive Heymann's nephritis in rats. Isoelectric focusing followed by immunoblotting of deoxycholate-soluble Fx1A antigens with the heterologous and autologous antibodies, indicated species differences in epitope recognition which could account for dissociation between the two models. 相似文献
28.
Tumor necrosis factor-alpha is expressed by glomerular visceral epithelial cells in human membranous nephropathy. 总被引:2,自引:1,他引:2
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T. J. Neale B. M. Rüger H. Macaulay P. R. Dunbar Q. Hasan A. Bourke R. P. Murray-McIntosh A. R. Kitching 《The American journal of pathology》1995,146(6):1444-1454
The role of tumor necrosis factor alpha (TNF-alpha) was examined in biopsy-proven glomerulonephritis by immunohistochemistry, in situ hybridization, immunogold electron microscopy, immunoassay in serum and urine, and urinary immunoblot. Striking glomerular capillary wall and visceral glomerular epithelial cell TNF-alpha protein staining was observed in all cases of membranous nephropathy and membranous lupus nephropathy. Staining was less frequently observed in crescentic glomerulonephritis and in isolated cases of other histological subtypes of glomerulonephritis, usually in association with glomerular macrophages. By immunogold electron microscopy TNF-alpha was localized in membranous nephropathy within the visceral glomerular epithelial cells, and also in the glomerular basement membrane, especially in relation to immune deposits. In situ hybridization localized TNF-alpha mRNA exclusively to glomerular epithelial cells in all biopsies with membranous morphology but not in other histological subtypes. Concentrations of TNF-alpha were significantly increased compared with normal controls in the urine of patients with membranous nephropathy and with crescentic glomerulonephritis. The expression of TNF-alpha by glomerular epithelial cells exclusively and universally in biopsies showing a membranous morphology strongly suggests this cytokine has a role in the pathogenesis of membranous nephropathy. 相似文献
29.
30.
Missense mutation in a von Willebrand factor type A domain of the alpha 3(VI) collagen gene (COL6A3) in a family with Bethlem myopathy 总被引:2,自引:0,他引:2
Pan TC; Zhang RZ; Pericak-Vance MA; Tandan R; Fries T; Stajich JM; Viles K; Vance JM; Chu ML; Speer MC 《Human molecular genetics》1998,7(5):807-812
The Bethlem myopathy is a rare autosomal dominant proximal myopathy
characterized by early childhood onset and joint contractures. Evidence for
linkage and genetic heterogeneity has been established, with the majority
of families linked to 21q22.3 and one large family linked to 2q37,
implicating the three type VI collagen subunit genes, COL6A1 (chromosome
21), COL6A2 (chromosome 21) and COL6A3 (chromosome 2) as candidate genes.
Mutations of the invariant glycine residues in the triple-helical
domain-coding region of COL6A1 and COL6A2 have been reported previously in
the chromosome 21-linked families. We report here the identification of a
G-->A mutation in the N-terminal globular domain-coding region of COL6A3
in a large American pedigree (19 affected, 12 unaffected), leading to the
substitution of glycine by glutamic acid in the N2 motif, which is
homologous to the type A domains of the von Willebrand factor. This
mutation segregated to all affected family members, to no unaffected family
members, and was not identified in 338 unrelated Caucasian control
chromosomes. Thus mutations in either the triple-helical domain or the
globular domain of type VI collagen appear to cause Bethlem myopathy.
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