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PubMed2001

Mitochondrial inheritance in Schistosoma mansoni: mitochondrial variable number tandem repeat mutation produces noise on top of the signal.

The Schistosoma mansoni mitochondrial genome contains tandemly arrayed copies of a 62-base repeat motif. The tandem array is highly polymorphic with respect to number of repeats and commonly exhibits heteroplasmy. This study shows that a very high rate of mutation rapidly produces new repeat lengths (new haplotypes) for this mitochondrial variable number tandem repeat. A maternal inheritance pattern is also demonstrated for this repeat sequence, while the high mutation rate causes some offspring to exhibit nonmaternal haplotypes. Frequent generation of new haplotypes can be observed within samples of clonal cohorts taken from monomiracidial snail infections. These same clonal cercarial groups, when crossed, produce F1 generations that exhibit the maternal set of haplotypes, across all individuals, with the frequent addition of new mutant haplotypes. In each of 2 crosses, a subset of the recently arisen haplotypes match paternal haplotypes by chance (30.4% and 18.8%), thus giving the false appearance of partial paternal inheritance of mitochondria.

Animals↗
PubMed1992

Genetics of spike-wave discharges in the electroencephalogram (EEG) of the WAG/Rij inbred rat strain: a classical mendelian crossbreeding study.

The WAG inbred strain might be an animal model for human absence epilepsy. To study the inheritance pattern of absence epilepsy, WAG rats were crossbred, in a classical Mendelian way, with inbred ACI rats which show no signs of epilepsy. In the parental strains, reciprocal F1 hybrids, F2, B1, and B2 generations, the number and duration of spike-wave discharges were determined. One hundred percent of the F1 animals showed spike-wave discharges, while the percentages for the F2, B1, and B2 generations were 79, 95, and 37%, respectively. These results suggest that the occurrence of spike-wave discharges is determined by one gene with a dominant mode of inheritance. Cavalli's least-squares fitting procedure suggested different genetic models for the two parameters (number and duration) during the two periods (dark and light). These results confirm our previous findings (Peeters et al., Behav. Genet. 20, 453-460, 1990) that a number of genes are involved in absence epilepsy. One dominant gene appears to determine the occurrence, however, while others manipulate the number and duration of epileptic phenomena during the two periods dark and light.

Animals↗
PubMed1994

Benign mitochondrial myopathy with decreased succinate cytochrome C reductase activity.

In most of the cases previously described, the defect on complex II was suggested by low activity of succinate cytochrome C reductase (SCCR). The clinical pattern of the previous 10 cases is heterogeneous and may be limited to one particular tissue or be of a more general nature. We report a 22-year-old-woman, daughter of consanguineous parents, with generalized muscle weakness, easy fatigability and benign course, who showed a decrease of SCCR activity in mitochondria of muscle fibers. Free carnitine (FC) concentration was decreased in muscle as well. The muscle biopsy showed a mild variation in fiber size, with fiber type I predominance, subsarcolemmal oxidative DPNH accumulations, excess of neutral lipids and abnormally large mitochondria with paracrystalline inclusions. A possible inheritance pattern is discussed. Coenzyme Q10 therapy in this patient induced a significant increase of global MRC index score and a decrease of the turns-mean amplitude ratio in the automatic analysis of the EMG.

Adult↗
PubMed1995

Inherited and noninherited risk factors in rheumatoid arthritis.

Rheumatoid arthritis (RA) is likely the result of a concerted action of several inherited and noninherited factors. Although there is a high suspicion that environmental factors are important, proof is missing. Most information has been collected on genetic risk factors. The inheritance pattern for RA is complex, and there is good evidence that HLA as well as non-HLA genes are involved. Almost all racial-ethnic groups share the association of RA with the HLA-DRB1-encoded sequence motif QKRAA or QRRAA. However, the completeness of the association varies significantly in different ethnic cohorts, as can be expected in a multigene model. The sequence motif translates into a pocket in the antigen-binding site of the HLA-DR molecule. The "rheumatoid pocket" accommodates peptide side chains and has distinct binding characteristics. Epidemiologic evidence points toward a role for non-HLA genes. Candidate genes, such as transporter in antigen processing (TAP) genes are currently explored. Major advances in defining and understanding the contribution of inherited and noninherited factors in RA may come from abandoning the concept of RA as a single entity and accepting a heterogeneity model for RA. Distributions of HLA-DR genes indicate that several subsets of RA patients exist. Seronegative (prognostically good) and seropositive (prognostically worse) patients can be distinguished by the arginine versus lysine substitution at position 71 of the HLA-DRB1 gene. A different dimension of disease, rheumatoid organ disease, appears to be reached in patients with two HLA-DRB1*0401 alleles. Identification of distinct RA subsets may allow us to stratify patients into categories that differ with respect to etiology, disease course, clinical pattern, and treatment response.

Amino Acid Sequence↗
PubMed2022

The evolutionary dynamics of extrachromosomal DNA in human cancers.

Oncogene amplification on extrachromosomal DNA (ecDNA) is a common event, driving aggressive tumor growth, drug resistance and shorter survival. Currently, the impact of nonchromosomal oncogene inheritance-random identity by descent-is poorly understood. Also unclear is the impact of ecDNA on somatic variation and selection. Here integrating theoretical models of random segregation, unbiased image analysis, CRISPR-based ecDNA tagging with live-cell imaging and CRISPR-C, we demonstrate that random ecDNA inheritance results in extensive intratumoral ecDNA copy number heterogeneity and rapid adaptation to metabolic stress and targeted treatment. Observed ecDNAs benefit host cell survival or growth and can change within a single cell cycle. ecDNA inheritance can predict, a priori, some of the aggressive features of ecDNA-containing cancers. These properties are facilitated by the ability of ecDNA to rapidly adapt genomes in a way that is not possible through chromosomal oncogene amplification. These results show how the nonchromosomal random inheritance pattern of ecDNA contributes to poor outcomes for patients with cancer.

Biological Evolution↗
PubMed1989

C8A and C8B polymorphisms in Norwegians and Norwegian lapps.

C8 inheritance patterns in 364 mother-child pairs formed the basis for evaluation of the existence of silent alleles (null alleles) in the genes determining the two known polymorphic C8 systems. While evidence for such alleles was not found in C8A (alpha-gamma complex), two observations of null allele segregation in C8B (beta chain) indicate a C8BQ*0 allele frequency of about 0.07. Two population samples comprising 150 Lappish and 1,264 non-Lappish Norwegians were examined for phenotype distributions in C8A and C8B. The phenotype distributions were mainly in accordance with the expected Hardy-Weinberg distribution. The results for C8A indicated simple, codominant inheritance of two frequent and several rare alleles. Allele frequencies were similar in the two populations. The C8A B gene frequency in Norwegians was significantly lower than that in FRG and higher than that in Negroes. C8B allele frequencies were also calculated from gene counts in the population material, but with due corrections for the C8BQ*0 frequency observed in the mother-child material.

Alleles↗
PubMed1994

A molecular approach to the stratification of cardiovascular risk in families with Marfan's syndrome.

BACKGROUND: The fibrillin gene encodes a protein in the extracellular matrix, and this protein is widely distributed in elastic tissues. The fibrillin gene is the site of mutations causing Marfan's syndrome. This disorder shows a high degree of clinical variability both between and within families. Each family appears to have a unique mutation in the fibrillin gene, which precludes the routine use of mutation screening for presymptomatic diagnosis of the disorder. The goal of this study was to develop a widely applicable method of molecular diagnosis. METHODS: We used three newly characterized intragenic sites of normal DNA repeat-sequence variation (i.e., polymorphisms) as markers to follow the inheritance pattern of specific copies (alleles) of the fibrillin gene in multiple kindreds with various clinical features of Marfan's syndrome. RESULTS: The polymorphic markers allowed identification of the particular copy of the fibrillin gene that cosegregated with Marfan's syndrome in 13 of the 14 families tested. In 11 families a definite presymptomatic diagnosis of Marfan's syndrome could be made in family members who had only equivocal manifestations of the disorder. In two other families, some family members demonstrated either classic Marfan's syndrome or a milder but closely related phenotype. The copy of the fibrillin gene that cosegregated with classic Marfan's syndrome was not inherited by family members with the latter, atypical, form of the disease. These milder phenotypes, previously diagnosed as Marfan's syndrome, were not associated with aortic involvement. CONCLUSIONS: These results document the usefulness of novel polymorphic DNA repeat sequences in the presymptomatic diagnosis of Marfan's syndrome. Our findings also demonstrate that the various clinical phenotypes seen in selected families may be due not to single fibrillin mutations, but rather to different genetic alterations. These findings underscore the need for a modification of the current diagnostic criteria for Marfan's syndrome in order to achieve accurate risk assessment.

Alleles↗
PubMed1984

Genetic studies in Parkinson's disease.

In a previous paper (2), we had demonstrated the existence of familial cases of Parkinson's disease. We have now identified two main patterns to these familial cases within our own clinical material. The total familial subgroup of 50 kinships that we report represents 13% of our 342 kinships personally examined in detail. Only 2 of these familial cases turn out to be phenocopies of Parkinson's disease. A further 34 kinships (10% of all Parkinson's disease) are classified within the essential-tremor related Parkinsonism subgroup that we have previously described and 10 kinships (3% of all Parkinson's disease) form what we now call the recessive akineto-rigid syndrome. A further 4 kinships (called pseudodominant) are probably examples of this same entity. These subgroups have quite distinct inheritance patterns and deserve more thorough metabolic investigations and clinical characterization. On the basis of these studies, we propose that a genetic type of Parkinson's disease be included in any classification of the disorder.

Genes, Dominant↗
PubMed1995

Mapping of genes predisposing to idiopathic generalized epilepsy.

Idiopathic generalized epilepsy (IGE) is characterized by recurring generalized seizures in the absence of detectable brain lesions and/or metabolic abnormalities. Twin and family studies suggest that genetic factors play a key part in IGE. A multilocus model appears to best fit the observed inheritance patterns. Mapping of IGE-related genes has been previously attempted using parametric methods, with conflicting results. In particular, recent evidence argues both for and against a chromosome 6p locus (EJM1) for juvenile myoclonic epilepsy, a subtype of IGE. We have approached the problem of mapping IGE loci using non-parametric methods, which have recently been successful for other complex diseases. No evidence for linkage to chromosome 6p was obtained. However, we obtained evidence for involvement of a locus at chromosome 8q24, close to the marker D8S256. The same 8q24 region was previously implicated in families with benign neonatal familial convulsions (BNFC), a generalized epilepsy syndrome that is inherited as a simple dominant mendelian trait. There is an apparent conserved syntenic group of genes in human 8q24 and a region of mouse chromosome 15, which harbors the stargazer (stg) locus. Homozygous mutant mice at the stg locus show a form of generalized epilepsy that resembles human absence epilepsy. Our findings may have implications for a locus on 8q24 predisposing to IGE.

Chromosome Mapping↗
PubMed1983

Multi-step genetic regulation of oncogene expression in fish hereditary melanoma.

Melanoma occurring spontaneously in Xiphophorus fish hybrids is a model system in which involvement of cellular oncogenes and multi-step regulation of their expression have been identified by classical genetics. The macromelanophore gene in platyfish (Xiphophorus maculatus) is a sex-linked codominant gene which determines the black spot patterns of macromelanophores in the skin. The macromelanophore locus includes a cellular oncogene which potentially induces neoplasms of the pigment cells. Expression of the oncogene is regulated by a multi-step genetic process and brings about a characteristic phenotype associated with pigment cell differentiation at each step. The multi-step genetic regulation of oncogene expression can be recognized by interspecific hybridization of the platyfish with swordtails (Xiphophorus helleri) which have not developed the macromelanophore gene. When platyfish are hybridized with swordtails, the F1 offspring carrying this gene develop a preneoplastic state. When the F1 offspring are back-crossed to swordtails, the backcross offspring develop a heritable form of melanoma with a characteristic inheritance pattern. This heritable form of melanoma occurs at an early age and has a well differentiated character. Thus, the first and second steps of oncogene expression bring about a preneoplastic state in the F1 offspring and a heritable form of melanoma in the backcross offspring, respectively. These steps may be due to progressive substitution of platyfish chromosomes with swordtail chromosomes in germ line cells, resulting in a progressive reduction of the dosage of regulatory genes in the platyfish genome. The third step of oncogene expression brings about a sporadic form of melanoma in the hybrid offspring bearing the preneoplastic state and heritable form of melanoma spontaneously or through induction by carcinogens. This form of melanoma has a poorly differentiated character. The incidence of this form is considerably enhanced by aging in adult life, thus exhibiting age-specific incidence. It is likely that this step is due to mutational events in regulatory genes, which occur in somatic cells following chromosome substitution in germ line cells by hybridization. The albino gene enhances the malignancy of the two forms of melanoma and the incidence of the sporadic form of melanoma, possibly by suppressing the differentiation of transformed pigment cells. These facts and speculations are summarized in Fig. 6. The molecular identification of oncogenes in this melanoma system and their transfer into the swordtail eggs may provide a useful means for studying oncogene expression during development, growth, and aging of animals.

Age Factors↗
PubMed1994

Retinal degeneration in motor neuron degeneration: a mouse model of ceroid lipofuscinosis.

PURPOSE: To evaluate the retinal degeneration of the motor neuron degeneration (mnd) mouse, and to confirm its inheritance pattern and gene location. METHODS: In screening the mnd/mnd mouse for ocular disease, a retinal degeneration was found that was evaluated by serial electroretinography, histology, electron microscopy, indirect ophthalmoscopy, and genetic and linkage analysis. RESULTS: In homozygous mnd mice, photoreceptor and outer nuclear layers show cell loss by 5 weeks after birth. By 2 months, the peripheral retina is preferentially thinner than central retina, and by 6 months the entire retina is reduced in thickness. The electroretinogram was extinguished by 6 months. Transmission electron microscopy at 3 and 6 months showed distinct cytoplasmic inclusions characteristic of the curvilinear profiles seen in human ceroid lipofuscinosis. Genetic analyses show that the retinal degeneration in mnd mice is inherited as a single autosomal gene with recessive expression, and a three-point cross placed the retinal degeneration at the mnd locus on the proximal end of mouse chromosome 8. Crosses with other known strains with retinal degeneration were normal. CONCLUSIONS. The mnd mouse model is similar to the juvenile onset Spielmeyer-Vogt form of ceroid lipofuscinosis (Batten disease), and provides a good model for the retinal degeneration found in these patients.

Alleles↗
PubMed2001

Inheritance of open-angle glaucoma in the Barbados family study.

The majority of genetic studies on open-angle glaucoma (OAG) have been conducted in primarily white populations, with investigations of inheritance patterns largely based on self-reported information. The Barbados Family Study of Open-Angle Glaucoma (BFSG) is the first study to investigate the transmission pattern(s) for OAG in a predominantly black population, based on standardized examinations. Each BFSG participant received a comprehensive examination including anthropometric and other measurements, best-corrected visual acuity, perimetry, tonometry, lens gradings, fundus photography, venipuncture, an extensive interview including ocular, medical and family history information and a comprehensive ophthalmologic evaluation. Conservative criteria were used to define glaucoma status, including the presence of both visual field defects and optic disc damage. The study included 207 OAG-affected probands (median age: 68 years) and 1,056 of their relatives (median age: 47 years). Among the relatives examined 10% (n = 106) had OAG and 13% (n = 141) had probable OAG. Segregation analyses were performed to determine the mode of inheritance for glaucoma in these families. The results indicate that transmission of OAG or probable OAG is most likely due to a major codominant gene. Both age and gender are shown to be significant factors as well; with an increase in risk being associated with each year of age over 54 years and an increase in risk for all ages and genotypes observed in males. These analyses do not, however, preclude the possible existence of an environmental component or other genetic determinants in OAG. Further evidence for the existence of a major gene may be obtained by additional follow-up of the relatively young cohort of relatives, as well as ongoing linkage analyses.

Adult↗
PubMed1988

Normal polymorphic variations and transcription of the decay accelerating factor gene in paroxysmal nocturnal hemoglobinuria cells.

In paroxysmal nocturnal hemoglobinuria (PNH), an acquired hemolytic anemia, deficiency of decay accelerating factor (DAF) renders blood cells susceptible to increased deposition of autologous complement activation fragments (C3b) and complemented-mediated injury. To investigate the mechanism of the DAF defect, DNA and mRNA from normal and PNH leukocytes were compared in blot hybridization assays by using DAF cDNA and oligonucleotide probes. Southern analyses of DNA from normal cells revealed a single gene spanning approximately equal to 35 kilobases of DNA. Six HindIII banding patterns were distinguishable among normal individuals. In family studies, the patterns segregated as three homozygous and three heterozygous genotypes deriving from three haplotypes: A, B, and C with frequencies of 0.47, 0.36, and 0.17, respectively. Oligonucleotide mapping localized the polymorphic HindIII sites to two noncoding regions in the vicinity of exons encoding (i) the protein oligosaccharide-rich domain and (ii) the mRNA 3'-untranslated region. Analyses of DNA from DAF-negative leukocytes of eight PNH patients demonstrated restriction fragment profiles identical to those of normal individuals for all enzymes studied. Three patients had the BC (normals = 3/32), three patients had the AA (normals = 6/32), and two patients had the AC (normals = 8/32) HindIII genotype. Of the three PNH patients exhibiting the BC genotype, family studies of two demonstrated the expected inheritance patterns, and RNA gel blot analyses of two showed mRNA transcripts indistinguishable from those in normal cells. The absence of DAF gene or mRNA alterations in affected PNH cells that lack other glycolipid-anchored proteins as well as DAF argues that the lesion underlying PNH cells resides in the glycolipid-anchor pathway.

Blood Proteins↗
PubMed1998

Linkage and allelic association of atopy and markers flanking the IL4-receptor gene.

BACKGROUND: Atopy, a clinical syndrome characterized by heightened IgE responsiveness, is largely determined by genetic factors. The disease may well be heterogeneous but the mode of inheritance is unknown. Several genes have been named which affected IgE responsiveness. However, results are conflicting reflecting heterogeneity and a complicated inheritance pattern of the atopic syndrome. In 1994 linkage of the 5q32 gene region and elevated total IgE levels were reported, leaving the IL4 gene as a prominent candidate. OBJECTIVES: We were interested in a possible involvement of the IL4-receptor gene in the development of atopy. METHODS: We employed sib-pair linkage analysis using highly polymorphic microsatellite markers within and flanking the IL4 receptor gene in atopic families, characterized for specific sensitization to inhalant allergens and elevated total serum IgE. Allele sizes were determined for all microsatellite probes to allow transmission disequilibrium analysis. RESULTS: We found significant sharing of maternal but not paternal alleles in affected sibs from two independent populations, both of which presented enhanced IgE responsiveness. Linkage and maternal inheritance could be confirmed by transmission disequilibrium analysis. CONCLUSIONS: We conclude from our findings that maternal inheritance of a gene in the chromosome 16p12 region increases the risk for enhanced IgE responsiveness. The most prominent candidate in this region is represented by the IL4 receptor gene.

Adolescent↗
PubMed1999

Familial patent ductus arteriosus and bicuspid aortic valve with hand anomalies: a novel heart-hand syndrome.

The association between cardiac and limb defects, particularly those affecting the hand, has been well documented by the delineation of several heart-hand syndromes. Based on observations with a three-generation family with seven affected individuals, we describe a novel heart-hand syndrome comprising patent ductus arteriosus, bicuspid aortic valve, 5th metacarpal hypoplasia, and brachydactyly. The inheritance pattern was consistent with autosomal dominance, although X-linked dominance could not be excluded. Penetrance appeared to be complete, but there was variability of the cardiac and hand phenotypes. Because this new syndrome closely resembled Char syndrome (patent ductus arteriosus, 5th finger middle phalangeal hypoplasia, and minor facial anomalies), multipoint linkage analysis was performed using polymorphic DNA markers spanning the recently identified Char syndrome critical region at chromosomal bands 6p12-p21.1. This analysis formally excluded this 3-cM region, documenting that the two traits are not allelic. In sum, a novel heart-hand syndrome involving left ventricular outflow and aortic arch as well as an ulnar ray derivative has been identified. Because the hand anomalies can be subtle, thorough evaluation is suggested for families inheriting these cardiac defects as a mendelian trait.

Alleles↗
PubMed1995

HLA disease associations: models for the study of complex human genetic disorders.

The genes of the human leukocyte antigen (HLA) region, the major histocompatibility complex (MHC) of humans, control a variety of functions involved in immune response and influence susceptibility to over 40 diseases. Theoretical studies in the development of models to determine the modes of inheritance of the HLA-associated diseases have led to a better understanding of the inheritance patterns in insulin-dependent diabetes mellitus (IDDM), rheumatoid arthritis, multiple sclerosis, ankylosing spondylitis, hemochromatosis, celiac disease, and others. It is now clear that many of the HLA-associated diseases involve heterogeneity in their HLA components, as well as non-HLA genetic factors. This review is presented using HLA-associated diseases, and in particular IDDM, as the example of interest, but the observations and techniques presented have direct relevance to the study of all human diseases with a complex genetic component. Three methods for localizing disease-predisposing genes are presented: (1) association studies, including population, family, and relative predispositional effects, (2) affected sib pair and other affected-relative methods, and (3) lod score analysis. A variety of complementary methods for studying the mode(s) of inheritance of the alleles at the disease-predisposing locus and for identifying the alleles and amino acids directly involved in the disease process also are presented.

Arthritis, Rheumatoid↗
PubMed2002

Clinical and molecular heterogeneity in the Brugada syndrome: a novel gene locus on chromosome 3.

BACKGROUND: Brugada syndrome is a form of idiopathic ventricular fibrillation characterized by a right bundle-branch block pattern and ST elevation (STE) in the right precordial leads of the ECG. Sodium channel blockers increase STE. Mutations of the cardiac sodium channel SCN5A cause the disorder, and an implantable cardioverter-defibrillator is often recommended for affected individuals. Mutations in other genes have not been identified, and it is not known if the efficacy of drug testing or the malignancy of arrhythmias correlates to the gene defect. METHODS AND RESULTS: We performed histories, physical examinations, ECGs, and drug testing on a large multigenerational family with Brugada syndrome. DNA isolated from blood samples, polymorphic genomic markers, and polymorphisms within candidate sodium channels were used for a genome-wide screen, fine mapping, and linkage analysis. We identified 12 affected individuals (right bundle-branch block, > or =1-mm STE) with an autosomal dominant inheritance pattern characterized by incomplete penetrance that appeared to be dependent on age and sex. Four affected individuals had syncope and 2 had documented ventricular arrhythmias, but there was minimal family history of sudden death. Procainamide infusions did not identify additional affected individuals. Linkage was present to an approximately equal 15-cM region on chromosome 3p22-25 (maximum LOD score=4.00). The sodium channel genes SCN5A, SCN10A, and SCN12A on chromosome 3 were excluded as candidates (LOD scores < or =-2). CONCLUSIONS: A Brugada syndrome locus distinct from SCN5A is associated with progressive conduction disease, a low sensitivity to procainamide testing, and a relatively good prognosis in a single large pedigree.

Adult↗
PubMed2001

Like mother, like daughter: evidence for non-genomic transmission of parental behavior and stress responsivity.

Considerable evidence demonstrates that the quality of the early environment influences patterns of development that, in turn, determine the health and productivity of the individual throughout their life span. However, the processes through which early life influences health are not clearly understood. Through the activation of the hypothalamo-pituitary-adrenal (HPA) axis and corticotropin-releasing hormone (CRH) pathways, prolonged or exaggerated responses to stress have profound effects on physiological and cognitive functions. Early maternal separation or handling of neonatal rats can program widespread and lifelong changes in various transmitter systems that regulate the HPA and CRH systems. Our studies show that a high level of maternal licking/grooming, and arched-back nursing correlates with reduced CRH mRNA expression and enhanced glucocorticoid negative feedback, and lower stress responses in the adult. This behavior is stably transmitted between generations and cross-fostering studies show that the offspring inherit the behavior from the nursing mother and not the biological mother. Such intergenerational transmission of maternal behavior is seen in rodents, primates and humans, and may underlie adaptive changes in the HPA axis. The neural basis of this inheritance pattern appears to reside in the central oxytocin system which determines features of maternal behavior. Through these various adaptive neural mechanisms the environmental demand on the mother is reflected in the quality of maternal care to her offspring. This, in turn, programs stress reactivity and maternal behavior patterns of the offspring. This not only determines certain health outcomes but also establishes the relationships between mother and offspring in the next generation. These findings suggest that for neurobiologists, the function of the family is an important level of analysis and the critical question is that of how environmental events regulate neural systems that mediate the expression of parental care.

Animals↗