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Dominantly inherited ataxias.

Molecular genetic studies in the past decade have demonstrated the enormous genetic heterogeneity among the dominantly inherited ataxias. Mutations at several distinct loci give rise to the progressive dominant ataxias and at least 2 different mutations cause episodic ataxias with dominant inheritance. The well-established genotypes for progressive dominant ataxias have all involved expansions of repeated CAG sequences. Clinically these patients present with progressive cerebellar deficits as well as signs relating to pathology in other neural systems in a variable fashion. Some of these other signs serve as diagnostic clues to the underlying genotype, but the identification of the genotype from the clinical phenotype alone is usually difficult. The CAG expansions involved usually are unstable with intergenerational expansions as well as contractions of the repeat size. Phenotypic features such as age of onset and to a lesser extent disease progression rate and the presence of specific clinical signs depend on the CAG repeat size. Identification of the mutations has allowed precise genotypic diagnosis in several families allowing more accurate genetic counseling, including predictive testing of at risk individuals when sought. Also, increasing information about the gene products and their abnormal distributions in disease brain is rapidly giving rise to rational ideas about the pathogenesis of neuronal degeneration in these diseases and raising hope for meaningful treatment strategies.

Ataxia↗

Approach to patients with inherited neurologic disorders.

There have been tremendous advances in our understanding of inherited neurologic disorders. It is important to recognize that genetic factors contribute to common neurologic disorders once considered idiopathic. Diagnosing and counseling individuals with inherited neurologic disorders requires understanding of fundamental genetic principles. The essential approach to such patients and their family members is presented.

Genetic Counseling↗

Mode of inheritance of decreased C3b receptors on erythrocytes of patients with systemic lupus erythematosus.

The erythrocytes of patients with systemic lupus erythematosus have been shown to have a decreased number of receptors for the major cleavage fragment of the third component of complement (C3b). We studied the basis for this decreased number of C3b receptors by measuring the uptake of anti-C3b-receptor antibody on cells from 113 normal subjects, 38 patients with systemic lupus erythematosus, 14 of their spouses, and 47 of their relatives. The normal subjects had 5014 +/- (mean +/- S.E.M.) receptor sites per cell, but the patients and their relatives had significantly fewer sites--2809 +/- 241 and 3167 +/- 196, respectively (P less than 0.0005). The number of sites in the patients' spouses did not differ from normal (P greater than 0.3). Three phenotypes, indicated by the numbers of receptors, occurred in the normal population; a high phenotype (HH, with 5500 to 8500 sites per cell), an intermediate phenotype (HL, with 3000 to 5499), and a low phenotype (LL, less than 3000). These three phenotypes were present in 34, 54, and 12 percent, respectively, of the normal subjects; in contrast, 5, 42, and 53 per cent of patients had these respective phenotypes. Pedigree analyses indicated that these phenotypes were inherited in an autosomal codominant manner. We conclude that the decreased number of C3b receptors in lupus is inherited, not acquired.

Adult↗

Inheritance pattern and clinical response to splenectomy as a reflection of erythrocyte spectrin deficiency in hereditary spherocytosis.

To determine how various inheritance patterns and responses to splenectomy relate to erythrocyte spectrin deficiencies in hereditary spherocytosis, we measured the spectrin content of erythrocytes by radioimmunoassay in 33 patients with this disease. Patients with the dominant form of hereditary spherocytosis generally had mild anemia, with spectrin at 63 to 81 percent of normal levels. Patients with the nondominant form of the disease had anemia ranging from severe to mild, with corresponding spectrin levels of 30 to 74 percent; their siblings were affected similarly. Distantly related homozygotes had different clinical severities with correspondingly different spectrin levels. The parents and offspring of patients with the nondominant form were clinically normal but consistently had subtle erythrocyte abnormalities. Spectrin levels in all patients were inversely related to osmotic fragility (P less than 0.0001), and they were also correlated with the clinical response to splenectomy: patients with spectrin levels above 70 percent achieved normal blood counts, those with levels of 40 to 70 percent had compensated hemolysis, and those with levels below 40 percent improved but remained anemic (P less than 0.0001). We conclude that the inheritance pattern and response to splenectomy in hereditary spherocytosis reflect erythrocyte spectrin deficiencies as determined by radioimmunoassay.

Anemia, Hemolytic, Congenital↗

An inherited defect in aldosterone biosynthesis caused by a mutation in or near the gene for steroid 11-hydroxylase.

The final step in aldosterone biosynthesis, an oxidation at position 18 of 18-hydroxycorticosterone, is catalyzed by an enzymatic activity termed corticosterone methyl oxidase II (CMO II). This activity is mediated in vitro by P450c11 (steroid 11-hydroxylase), a cytochrome P-450 enzyme that also catalyzes the preceding two steps of 11-hydroxylation and 18-hydroxylation. CMO II deficiency, an inherited defect in the 18-oxidation step, impairs aldosterone biosynthesis and thus leads to a clinical syndrome of salt wasting. To test the hypothesis that CMO II deficiency results from a mutation affecting the structural gene for P450c11, we examined 11 affected and 21 unaffected members of six families with this disorder. After DNA samples were digested with the restriction endonuclease MspI (thereby cutting the DNA at specific sites) and hybridized with a P450c11 DNA probe, a unique DNA fragment in the P450c11 structural gene was detected in subjects with the deficiency. The DNA fragment and the disease trait were inherited together in each family, demonstrating that CMO II deficiency is caused by a mutation in or very near the structural gene for P450c11 on chromosome 8. We conclude that the metabolic diseases of CMO II and 11-hydroxylase deficiency, which have distinct clinical symptoms, may be caused by different mutations in the single gene for a multifunctional enzyme.

Aldosterone↗

Paternally inherited inactivating mutations of the GNAS1 gene in progressive osseous heteroplasia.

BACKGROUND: Progressive osseous heteroplasia (POH), an autosomal dominant disorder, is characterized by extensive dermal ossification during childhood, followed by disabling and widespread heterotopic ossification of skeletal muscle and deep connective tissue. Occasional reports of mild heterotopic ossification in Albright's hereditary osteodystrophy (AHO) and a recent report of two patients with AHO who had atypically extensive heterotopic ossification suggested a common genetic basis for the two disorders. AHO is caused by heterozygous inactivating mutations in the GNAS1 gene that result in decreased expression or function of the alpha subunit of the stimulatory G protein (Gsalpha) of adenylyl cyclase. METHODS: We tested the hypothesis that GNAS1 mutations cause POH, using the polymerase chain reaction to amplify GNAS1 exons and exon-intron boundaries in 18 patients with sporadic or familial POH. RESULTS: Heterozygous inactivating GNAS1 mutations were identified in 13 of the 18 probands with POH. The defective allele in POH is inherited exclusively from fathers, a result consistent with a model of imprinting for GNAS1. Direct evidence that the same mutation can cause either POH or AHO was observed within a single family, in which the phenotype correlated with the parental origin of the mutant allele. CONCLUSIONS: Paternally inherited inactivating GNAS1 mutations cause POH. This finding extends the range of phenotypes derived from haplo insufficiency of GNAS1, provides evidence that imprinting is a regulatory mechanism for GNAS1 expression, and suggests that Gsalpha is a critical negative regulator of osteogenic commitment in nonosseous connective tissues.

Base Sequence↗

Inherited perforin and Fas mutations in a patient with autoimmune lymphoproliferative syndrome and lymphoma.

A 27-year-old man with the autoimmune lymphoproliferative syndrome and a large-B-cell lymphoma had heterozygous mutations in the Fas and perforin (Prf1) genes. The Fas mutation was inherited from his healthy father and was also carried by his healthy brother, whereas the Prf1 mutation was inherited from his healthy mother. The combined effect of the two mutant genes may have contributed to the development of the autoimmune lymphoproliferative syndrome and lymphoma in this patient.

Adult↗

Type II collagen gene variants and inherited osteonecrosis of the femoral head.

BACKGROUND: Avascular necrosis of the femoral head (ANFH) causes disability that often requires surgical intervention. Most cases of ANFH are sporadic, but we identified three families in which there was autosomal dominant inheritance of the disease and mapped the chromosomal position of the gene to 12q13. METHODS: We carried out haplotype analysis in the families, selected candidate genes from the critical interval for ANFH on 12q13, and sequenced the promoter and exonic regions of the type II collagen gene (COL2A1) from persons with inherited and sporadic forms of ANFH. RESULTS: We identified a G-->A transition in exon 50 of COL2A1 in affected members of a four-generation family with ANFH. This transition predicts the replacement of glycine with serine at codon 1170 in a GXY repeat of type II collagen. Another pedigree was shown to harbor the same transition, but the mutant allele occurred on a different haplotype background. In a third family, a G-->A transition in exon 33 of the gene, causing a glycine-to-serine change at codon 717, was detected. No mutation was found in the COL2A1 coding region in sporadic cases of ANFH. CONCLUSIONS: All the patients with familial ANFH whom we studied carried COL2A1 mutations. In families with ANFH, haplotype and sequence analysis of the COL2A1 gene can be used to identify carriers of the mutant allele before the onset of clinical symptoms, allowing the initiation of measures that may delay progression of the disease.

Adult↗

Reticulate acropigmentation of Dohi: a case report of autosomal recessive inheritance.

Reticulate acropigmentation of Dohi is a rare dyschromic disorder that generally has an autosomal dominant pattern of inheritance. Most of the cases have primarily been described from Japan. Only a few similar cases have been described elsewhere. We describe 3 black siblings, one boy and two girls, who had progressive reticulate hyperpigmented and hypopigmented macules over the dorsa of hands and feet, which began in early childhood. There were no palmar pits or breaks of the epidermal rete ridge pattern nor was there a family history of any pigmentary skin diseases. Three skin biopsies were performed on one patient; a biopsy specimen from a hyperpigmented macule showed increased melanin in all epidermal levels tapering towards the surface, a second biopsy specimen from a hypopigmented macule showed much less melanin, but it had a similar distribution. A third specimen from a hyperpigmented macule for electron microscopy showed a moderate number of stage III and IV melanosomes in the cytoplasm of the melanocytes. To our knowledge, these patients are the first cases reported from the Middle East with an autosomal recessive pattern of inheritance, confirming previous reports.

Adolescent↗

Maternal and fetal inherited thrombophilias are not related to the development of severe preeclampsia.

OBJECTIVE: Thrombotic vascular disease may predispose patients to the development of preeclampsia. The purpose of this study was to determine whether maternal or fetal genotype frequencies of the inherited thrombophilic gene mutations (factor V Leiden, methylenetetrahydrofolate, and prothrombin) are altered in severe preeclampsia. STUDY DESIGN: We performed a prospective cross-sectional study to compare the maternal and fetal genotype frequencies of factor V Leiden, methylenetetrahydrofolate, and prothrombin. One hundred ten patients with severe preeclampsia were matched for gestational age to 97 normotensive pregnancies. Umbilical cord blood was obtained from 92 control patients and 75 patients with preeclampsia. Deoxyribonucleic acid was extracted from leukocytes and polymerase chain reaction was performed. Polymerase chain reaction products were digested with the appropriate restriction enzyme and fractionated by gel electrophoresis. Genotype frequencies were calculated. Statistical significance was determined by the chi(2) test. RESULTS: There were no significant differences between patients with severe preeclampsia and control patients regarding frequency of maternal factor V Leiden G/506/A mutation (4.4% vs 4.3%; P =.96), methylenetetrahydrofolate CC/667/TT mutation (9.6% vs 6.3%; P =.54), or prothrombin G/20210/A mutation (0% vs 1.1%; P =.92). In addition, no statistical difference could be found between fetal thrombophilias and the development of preeclampsia. Findings were similar in both white (n = 47) and African American (n = 63) preeclamptic subsets. Moreover, there was no association between any of the maternal or fetal genetic polymorphisms and the incidence of hemolysis, elevated liver enzymes, and low platelet count syndrome (n = 21); eclampsia (n = 12); or intrauterine growth restriction (n = 9). CONCLUSION: Inherited thrombophilias are not associated with severe preeclampsia.

Adult↗

Bcl-2 overexpression corrects mitochondrial defects and ameliorates inherited desmin null cardiomyopathy.

One of the hallmarks of cardiomyopathy and heart failure is pronounced and progressive cardiomyocyte death. Understanding the mechanisms involved in cardiomyocyte cell death is a topic of great interest for treatment of cardiac disease. Mice null for desmin, the muscle-specific member of the intermediate filament gene family, develop cardiomyopathy characterized by extensive cardiomyocyte death, fibrosis, calcification, and eventual heart failure. The earliest ultrastructural defects are observed in mitochondria. In the present study, we have demonstrated that these mitochondrial abnormalities are the primary cause of the observed cardiomyopathy and that these defects can be ameliorated by overexpression of bcl-2 in desmin null heart. Overexpression of bcl-2 in the desmin null heart results in correction of mitochondrial defects, reduced occurrence of fibrotic lesions in the myocardium, prevention of cardiac hypertrophy, restoration of cardiomyocyte ultrastructure, and significant improvement of cardiac function. Furthermore, we have found that loss of desmin also diminishes the capacity of mitochondria to resist exposure to calcium, a defect that can be partially restored by bcl-2 overexpression. These results point to a unique function for desmin in protection of mitochondria from calcium exposure that can be partially rescued by overexpression of bcl-2. We show that bcl-2 cardiac overexpression has provided significant improvement of an inherited form of cardiomyopathy, revealing the potential for bcl-2, and perhaps other genes in the family, as therapeutic agents for heart disease of many types, including inherited forms.

Animals↗

A mitotically inheritable unit containing a MAP kinase module.

Prions are novel kinds of hereditary units, relying solely on proteins, that are infectious and inherited in a non-Mendelian fashion. To date, they are either based on autocatalytic modification of a 3D conformation or on autocatalytic cleavage. Here, we provide further evidence that in the filamentous fungus Podospora anserina, a MAP kinase cascade is probably able to self-activate and generate C, a hereditary unit that bears many similarities to prions and triggers cell degeneration. We show that in addition to the MAPKKK gene, both the MAPKK and MAPK genes are necessary for the propagation of C, and that overexpression of MAPK as that of MAPKKK facilitates the appearance of C. We also show that a correlation exists between the presence of C and localization of the MAPK inside nuclei. These data emphasize the resemblance between prions and a self-positively regulated cascade in terms of their transmission. This thus further expands the concept of protein-base inheritance to regulatory networks that have the ability to self-activate.

Alleles↗

Hepatitis and Australia antigen: autosomal recessive inheritance of susceptibility to infection in humans.

Examples of inherited susceptibility to infection controlled by genes segregating at one or a small number of loci have been identified in lower animals. In this study we report data on what appears to be a similar situation in humans. "Australia antigen" is an antigen found in the sera of patients with acute and chronic hepatitis, and it may actually be a form of virus. It is very common in many tropical areas, and people in these areas having the antigen appear to be hepatitis carriers. The antigen is detected by immuno-diffusion in agar gel (Ouchterlony method). Individuals with the antigen are designated Au(1) and those without it Au(0). Family studies involving 1797 different individuals residing on the island of Bougainville are consistent with the hypothesis that susceptibility to chronic infection with the "antigen" is controlled by an autosomal recessive gene (Au(1)). This confirms the conclusions previously arrived at from similar (but less extensive) studies on the island of Cebu. Individuals with this inherited susceptibility do not ordinarily have overt manifestations of hepatitis. The sign test was used to determine family clustering. Segregation analysis was performed by the method of C. A. B. Smith. In the 41 Au(0) x Au(0) matings, 53.8 recessives were expected in the offspring and 56 were seen (0.7 > p > 0.5). In the Au(1) x Au(0) matings, 40.1 recessives were expected and 42 were seen (0.7 > p > 0.5). The Au(0) x Au(0) matings were also analyzed by the method of Li and Mantel, in which the recessive ratio of 0.25 is expected by the genetic hypothesis. The values observed were 0.2527 for the Bougainville study and 0.2461 for the Cebu study.

Antigens↗

Two independently inherited electrophoretic variants of the lysine-rich histones of maize (Zea mays).

We report here the first instance of inherited intraspecific histone variation in plants. Maize lysine-rich histone I is composed of four subfractions that are electrophoretically distinct in long polyacrylamide gels. Initial segregation studies indicate that at least one subfraction shows mobility differences inherited as if controlled by a single Mendelian locus. The locus is not on the short arms of chromosomes 2 or 4. The third subfraction also shows variants. Indirect evidence indicates that the genes controlling the variants of this subfraction segregate independently of those of the first. We suggest the symbols alh-A188 and alh-W23 to designate two of the alleles we have discovered of the first subfraction (a) of the lysine-rich histones and clh-A188 and clh-W23 the alleles of the third subfraction (c) of the lysine-rich histones. Other strains of maize show other differences in their histone I fractions, suggesting that there is inbredline-specific polymorphism with respect to histone I variants. The meiotic chromosome mutants, elongate and sticky, do not appear to condition maize histone alterations that can be detected electrophoretically.

Alleles↗

Inheritance of killer phenotypes and double-stranded RNA in Ustilago maydis.

Three different killer specificities in U. maydis are inherited cytoplasmically and transmitted by cell fusion. Each killer generates low frequencies of specifically immune forms in crosses with sensitive strains. The properties of immunity to each killer are also inherited cytoplasmically and transmitted by cell fusion. Killer strains carry virus-like particles about 41 nm in diameter. Each killer possesses distinct double-stranded RNA components that range in molecular weight from 0.46 X 10(6) to 2.9 X 10(6). Two components are shared by all three killers. Immune strains possess new forms. Crosses and heterokaryons between different killers revealed unilateral or mutual restrictions that prevent inclusion of two killer specificities in the same cell.

Basidiomycota↗

Inheritance of selected pathotoxin resistance in maize plants regenerated from cell cultures.

Texas male-sterile cytoplasm (cms-T) maize is susceptible to Helminthosporium maydis race T and its pathotoxin, whereas nonsterile cytoplasm maize is resistant. Callus cultures initiated from immature embryos of a cms-T genotype, BC(1)A188(T), were susceptible to the toxin and were capable of plant regeneration. Toxin-resistant cell lines were selected by a sublethal enrichment procedure in which cms-T callus was grown for several selection cycles (subculture transfers) in the presence of progressively higher concentrations of toxin. Periodically during the selection process, plants were regenerated from the cms-T cultures to determine their susceptibility or resistance to the toxin. Plants regenerated after four cycles of selection were male-sterile and toxin-susceptible as shown by leaf bioassays. All plants regenerated from cell lines isolated from the fifth selection cycle onward, however, were toxin-resistant and 52 of 65 were fully male-fertile. The remaining 13 "male-sterile" resistant plants did not shed pollen and did not resemble cms-T plants in tassel morphology. Some "male-sterile" plants produced anthers containing a small amount of starch-filled pollen, suggesting that the sterility of these 13 plants was not the result of the cms-T trait. Leaf bioassays on F(1) progeny from regenerated resistant plants indicated that resistance to the toxin was inherited only through the female. The male-fertility trait also was inherited only through the female. After inoculation with H. maydis race T spores, leaf lesion size for progeny from regenerated resistant plants coincided with their reaction to the toxin. This result indicated that plant resistance to the pathogen was closely correlated with the toxin resistance obtained through cell culture selection.

Journal Article↗

Defective organization of actin in cultured skin fibroblasts from patients with inherited adenocarcinoma.

In the cytoplasm of well-spread cultured normal fibroblasts, actin is organized into a network of cables that run the length of the cell just inside the adherent cell membrane. A diffuse matrix replaces the cables in fibroblasts that have become tumorigenic as a result of oncogenic transformation. We have found a similar disruption in actin organization in cultured skin fibroblasts (passage 6-10) obtained by biopsy from patients with the inherited colonic cancer, adenomatosis of the colon and rectum (ACR). Because ACR is inherited as an autosomal dominant trait, about half the children of ACR patients will develop colon cancer, but they typically remain asymptomatic until at least the second decade of life. Actin distribution within cultured cells from children of ACR patients was identical either to that seen in cultured cells from normal persons or to that seen in cultured cells from ACR patients. The two different patterns were independent of age, sex, drug treatment, or infections of the donors. Apparently, this class of colonic carcinoma is accompanied by a systemic aberration in the organization of fibroblast cytoplasm, and this aberration can be detected by immunofluorescent localization of actin within cultured skin fibroblasts, prior to manifestation of any colonic symptoms.

Actins↗

Inheritance of chloroplast DNA in Chlamydomonas reinhardtii.

Two symmetrically located deletions of approximately 100 base pairs each have been identified in chloroplast DNA of Chlamydomonas reinhardtii. Although present in a mutant strain that requires acetate for growth, both deletions have been shown to be distinct from the nonphotosynthetic phenotype of this strain. These physical markers in the chloroplast genome and maternally inherited genetic markers showed strict cotransmission in reciprocal crosses. Thus, our results are consistent with the location of the well-characterized maternally inherited genetic markers in chloroplast DNA of C. reinhardtii.

Journal Article↗