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At least 19 recordsLinked to original sources
PubMed1975

Cytoplasmic inheritance in Saccharomyces cerevisiae: comparison of first zygotic budsite to mitochondrial inheritance patterns.

Zygotic first budsite in Saccharomyces cerevisiae was studied in relation to defined mitochondrial inheritance systems: both petite and drug resistance. It was hypothesized that a highly asymmetric inheritance pattern would be correlated to a high frequency of first budsites on the petite or drug resistant end of the zygote (i.e., that portion of the zygote which was originally the drug resistant or petite haploid before zygote formation). The data collected did not support the hypothesis. For drug resistance, the budsite pattern is identical for a highly biased and a moderately biased inheritance pattern. In a grande by grande cross there is a high probability of the first bud appearing on the conjugation bridge, with lower but equal probabilities of the first bud appearing on one end or the other of the zygote. A grande by petite cross changes this pattern to a high probability of the first bud appearing on the grade end of the zygote, with a lesser probability of the first bud appearing on the conjugation bridge and virtually no budding of the petite end. This phenomenon is independent of degree of neutrality or suppressiveness of the petite strain used, however. The difference between a grande and a grande by petite pattern may be due to the relative functional ability of the mitochondria in each end of the zygote. Tests using antimitochondrial drugs suggest that selection of first budsite on a zygote is a complex phenomenon, not simply dependent upon mitochondrial phenotype. In conclusion, selection of the first zygotic budsite appears to be independent of mitochondrial inheritance patterns.

Cell Division↗
PubMed1986

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↗
PubMed1976

Glucose-6-phosphate dehydrogenase of Biomphalaria glabrata (Say , 1818) (Mollusca: Pulmonata). Characterization and inheritance pattern.

Glucose-6-phosphate dehydrogenase of Biomphalaria glabrata has been characterized by electrophoresis, kinetic properties and inheritance pattern. It exists as a single electrophoretic band with no polymorphism in the natural population studied during the present investigations. There are no organ-specific differences in electrophoretic pattern. The enzyme from the homogenates of various organs e.g., albumen gland, digestive gland, ovotestis and columellar muscle show similar physico-chemical parameters, such as optima for pH, NADP and glucose-6-phosphate. Incorporation of NADP is essential for maintaining the stability of the enzyme, failing which, there appear artifactual variations in electrophoretic mobility of the enzyme. The apparent lack of polymorphism in natural population of Biomphalaria glabrata has been discussed.

Animals↗
PubMed1976

Cytoplasmic inheritance in Saccharomyces cerevisiae: comparison of zygotic mitochondrial inheritance patterns.

Mitochondrial movements in Saccharomyces cerevisiae (Sc) zygotes were monitored with phase-contrast microscopy and compared to known mitochondrial inheritance systems. The mitochondria of Sc were convincingly identified by integrated use of phase-contrast, cytochemical and electron microscopic observations. Mitochondria in Sc appear to move by saltatory jumps, which appear to be oriented towards movement of mitochondria into developing buds. Tracking of mitochondria of different genotypes was made possible by positive identification of each mitochondrial population before zygosis, and by the low degree of mixing (less than 10%) of mitochondrial populations before first bud septation. A grande by grande cross demonstrated equal numbers of mitochondria from each haploid moving into the first zygotic bud. A grande by neutral petite cross gave a 2:1 ratio of grande to petite mitochondria. However, a grande by suppressive petite cross gave equal numbers of grande and petite mitochondria. Using drug resistance systems, a comparison was made of highly biased (97%) and moderately biased (71%) chloramphenicol resistant inheritance patterns. In both cases, the ratios of drug resistant to sensitive mitochondria were 1:1. When numbers of mitochondria moving into an individual bud were compared to the phenotypic content of the clone of that bud, no model could be constructed which could predict the latter from the former. The data indicate (with the exception of the neutral petite by grande cross) that the numbers of each mitochondrial type "inserted" into the first zygotic bud are equal, regardless of the degree of asymmetry of inheritance of mitochondrial markers.

Chloramphenicol↗
PubMed1991

Caries susceptibility in inbred mouse strains and inheritance patterns in F1 and backcross (N2) progeny from strains with high and low caries susceptibility.

We studied dental caries susceptibility in various inbred mice strains infected with Streptococcus mutans and the inheritance pattern in the F1 and the N2 backcross animals. A high caries score was observed in four laboratory strains, BALB/cAJcl, C57BL/6NJcl, C57BL/10Slc and DBA/2NJcl. Three strains, C3H/HeNJcl, AKR/JSlc and CBA/JNCrj, showed less caries. Males of strain C57BL/10Slc (mean caries score = 112.2) and females of strain C3H/HeNJcl (mean caries score = 24.0) were chosen for examinations of the inheritance of the caries susceptibility. The mean caries score in (C57BL/10Slc x C3H/HeNJcl) F1 hybrids was 98.4, demonstrating that F1 progenies were susceptible. A number of N2 mice were obtained by mating the F1 male and the C3H/HeNJcl female. The caries scores of these N2 male mice had an extensive range, from 14 to 194. Assuming that a caries score over 74 (median of the scores between C57BL/10Slc and C3H/HeNJcl) belonged to the highly caries-susceptible group, N2 mice could be divided into groups with low or high caries susceptibility. Furthermore, the effect of nu/nu mutation on caries susceptibility in mice was also examined.

Analysis of Variance↗
PubMed1987

Patterns of inheritance of colonic polyps.

While the inheritance pattern of familial polyposis coli is established as an autosomal dominant pattern, the expression of the various extracolonic manifestations associated with the neoplastic polyposis is less well understood. The discrete polyp cancer syndrome may not be recognized unless both polyps and colon cancer are considered in the inheritance pattern. The hamartomatous polyps follow a Mendelian-dominant inheritance pattern for the Peutz-Jeghers syndrome, while the inheritance pattern for the juvenile polyposis syndromes is less clear. Cowden's disease appears in a Mendelian dominant pattern, but the occurrence of colonic polyps is less well documented. The ganglioneuromas follow a mendelian dominant inheritance pattern, while the relationship and occurrence of colonic polyps in association with Torre's syndrome is uncertain. The Mendelian dominant inheritance pattern for the cancer family syndrome is documented; the role of colon polyps in this syndrome is less well understood. A further understanding of the inheritance patterns of these various colon polyps will lead to more understanding of the basic disease and help in prevention and early detection for treatment and cure.

Adenomatous Polyposis Coli↗
PubMedDate not supplied

Esterases in the house fly. Polymorphisms and inheritance patterns.

Polyacrylamide gel electrophoresis was used to examine the variability and inheritance of esterases in five strains of the house fly, Musca domestica L. Individual zymograms exhibited 8 to 15 bands that could be assigned to one of five zones designated as A through E from anode to cathode. Correlations of P1-F1 banding patterns indicated the existence of at least 3 different loci in zone A. 2 each in zones B and C, and 4 in zone D; no clear inheritance patterns were discernable for the bands of zone E. Only the Es-5 locus of zone C was monomorphic in all of the strains studied. Eight loci possessed null alleles and codominant alleles were detected at six loci. The results suggest that esterases should prove useful for measuring relationships among fly populations or for various studies of population dynamics.

Alleles↗
PubMed2026

Spatial inheritance patterns across maize ears are associated with alleles that reduce pollen fitness.

Often, more pollen grains land on recipient flowers than there are ovules to fertilize. Consequently, the haploid male gametophyte engages in post-pollination competition, one way that pollen genotype can influence inheritance. The maize (Zea mays subsp. mays L.) inflorescence (ear), with its elongated stigma and style structures (silks), has a conspicuous spatial heterogeneity, with longer silks at the base of the ear than at the apex. To evaluate the hypothesis that alleles with reduced pollen fitness influence the spatial distribution of progeny genotypes along the ear, we developed an updated phenotyping platform that maps fluorescently marked mutant (Ds-GFP) kernel phenotypes on the ear via an implementation of the Faster R-CNN machine vision model (EarVision.v2) and a statistical pipeline that evaluates the relationship between kernel position and transmission ratio (EarScape). Our dataset (1384 ears) represents 58 Ds-GFP insertion alleles. None of the 48 alleles with Mendelian inheritance showed any significant spatial trend. In contrast, 50% of alleles with a pollen-specific transmission defect (5/10) exhibited significant spatial effects. An insertional mutant of the gene encoding a putative actin-binding protein, base-to-apex gradient1* (bag1*), is associated with decreased mutant transmission at the ear base relative to the apex. Surprisingly, a mutant allele of another pollen-expressed gene (Zm00001eb236740) generates the opposite trend, decreased mutant transmission toward the ear apex; and two mutant alleles of the sperm cell attachment factor gamete expressed2 (gex2) can produce ears with transmission highest at both base and apex. We conclude that pollen fitness mutants cause unexpectedly diverse spatial patterns of progeny genotypes.

Zea mays↗
PubMed1977

Aglossia-adactylia syndrome (special emphasis on the inheritance pattern).

Three cases, one with aglossia-adactylia and two with aglossia, are presented, all of whom were born to consanguineous families. Although none of the cases had similarly affected sibs, the possibility of the autosomal recessive mode of inheritance might be taken into account in this syndrome. The dermatoglyphic findings in one previously reported patient showed great similarity to those of one of our cases.

Abnormalities, Multiple↗
PubMed1977

Inheritance patterns in recurrent aphthous ulcers: twin and pedigree data.

Nineteen sets of twins and 318 individuals from six families were examined and interviewed in order to ascertain whether a genetic component could be established for recurrent aphthous ulcers (RAU). While no specific mode of inheritance could be established, the data strongly support the hypothesis of a genetic factor involved in susceptibility to the disease.

Diseases in Twins↗
PubMed1991

A c-myc gene variant without exon 1 and with an abnormal methylation pattern inherited in a woman with no evidence of malignancy.

A c-myc DNA with a deletion which includes 5' flanking, exon 1 and intron I sequences has been found in normal white blood cells of a mother and one daughter in a Northern Italian family. In addition, the degree of methylation of specific CCGG sites in the truncated DNA is lower in both mother and daughter than that found in normal DNA. It is of interest that deletions of the first exon and hypomethylation of the c-myc gene have usually been observed only in some neoplasias. However, our results demonstrate that the c-myc truncated DNA with the abnormal methylation pattern here reported is a genomic variant which by itself is not related to neoplastic transformation.

Chromosome Deletion↗
PubMed1992

The immune response to hepatitis B vaccine in humans: inheritance patterns in families.

We have recently shown that the human antibody response to the hepatitis B virus surface antigen (HBsAg) vaccine is major histocompatibility complex (MHC) associated. In studies of nonresponders to the vaccine, we found an increased incidence of individuals homozygous for human histocompatibility leukocyte antigen (HLA) proteins associated with the extended (conserved) haplotype [HLA-B8,SC01,DR3]. In later prospective vaccination trials, we showed that none of five individuals homozygous for this haplotype developed more than 1,300 radioimmunoassay (RIA) units of antibody (mean, 467 RIA units), while all heterozygotes made at least 2,500 RIA units (mean antibody level, 15,608 units). Our results suggested that [HLA-B8,SC01,DR3] lacks an immune response gene for HBsAg, and that response is inherited in a dominant fashion. To provide further evidence for this hypothesis, we have now analyzed the results of HBsAg immunization in families. 43 members of 10 families were immunized with the hepatitis B vaccine, including seven families where at least one member bore the haplotype [HLA-B8,SC01,DR3], and three families where one member had already received, but failed to respond to, the vaccine. In two of these three families, the presence of [HLA-B8,SC01,DR3] was subsequently found. Of nine MHC-identical sibling pairs in the study, both members of eight pairs had similar antibody responses (five nonresponder and three responder pairs). In all families with such sibling pairs, including the discordant pair, rank-ordering members by antibody level demonstrated that no relative's value came between the sibling pair values. Furthermore, of nine [HLA-B8,SC01,DR3]-haplotype-homozygous individuals, six were nonresponders, and two others had only low-normal responses. [HLA-B8,SC01,DR3]-heterozygous family members always had higher levels of antibody than their homozygous relatives. Linkage analysis of nonresponse to HLA haplotypes revealed a maximum likelihood LOD (logarithm of the odds) score of 6.3 at a recombination fraction of 0.1. The MHC association with lack of antibody response to HBsAg was not seen with tetanus immunization, where 1 of 20 HBsAg responders and 1 of 21 poor or nonresponders had tetanus titers of less than 1:512; both tetanus nonresponders were [HLA-B8,SC01,DR3] heterozygotes. Our results indicate that: (a) response to the HBsAg vaccine is MHC linked, and inherited in a dominant fashion; (b) an abnormal or missing immune response (Ir) gene for HBsAg is a characteristic of most examples of the extended haplotype [HLA-B8,SC01,DR3]; and (c) other haplotypes also have abnormal or missing Ir genes for HBsAg.

Female↗
PubMedDate not supplied

Polymorphisms and inheritance patterns of tetrazolium oxidase and octanol dehydrogenase in the house fly.

Zymogram analyses suggested the existence of two autosomal codominant alleles each at loci controlling the production of tetrazolium oxidase (To1) and octanol dehydrogenase (Odh1) in Texas house flies; an additional variant of the To1 locus was detected in a population from South Dakota. The allozymes of both systems may be dimeric as indicated by the presence of possible heteropolymers in flies heterozygous for To1 and Odh1 allels. Apparent nonsegregating isozymes of To and Odh (To2 and Odh2) were also noted in the zymograms of Texas flies. Some banding forms in the Odh gels could not be interpreted genetically.

Alcohol Oxidoreductases↗
PubMed1978

Unusual type of neural muscular atrophy with a possible X-chromosomal inheritance pattern.

In a large family five affected males belonging to four different kinships exhibited a muscle wasting of varying degree and with a predominantly proximal distribution. The index case had a facio-scapulo-humeral and peroneal muscular atrophy, whereas one of his cousins suffered a more generalized involvement starting in infancy and similar to Werdnig-Hoffman disease. The other affected family members had only slight changes. The index case and his affected brother had a positive Babinski sign. In enzyme histochemical preparations, specimens from the index case showed small group atrophy of type 2 fibers along with pseudomyopathic changes (whorled and coiled fibers, splitting) of type 1 fibers. Similar findings were observed in his cousin. Ultrastructural investigation gave no further information. Since all patients were males and the offspring of unaffected sisters, an X-chromosomal mode of transmission is proposed for this illness.

Adolescent↗
PubMed1978

Congenital absence of teeth: a review with emphasis on inheritance patterns.

Congenital absence of teeth is a heritably phenomenon probably most often passed to each generation by an autosomal dominant pattern with incomplete penetrance and variable expressivity. Correlation of hypodontia with systemic disease leads to the hypothesis that this frequent dental anomaly may in some cases be a microform of systemic ectodermal dysplasia.

Anodontia↗