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Results for “Inheritance Patterns”

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At least 73 records · Page 4Linked to original sources
PubMed1996

Inheritance patterns of new genetic markers and occurrence of spontaneous mosaicism in the monogenic blowfly Chrysomya rufifacies (Diptera:Calliphoridae).

Four new genetic markers for Chrysomya rufifacies, a fly with maternal sex determination, were characterized. The markers include one body colour mutant, black body (bl), and three eye colour mutants, brown eye (br), apricot eye (ap), and red eye (wr). Two of the latter, br and wr, turn out to be sex linked, the others behave as autosomal genes belonging to different linkage groups. wr is a hypomorphic and w an apomorphic mutation of the white gene, w/w is epistatic to br/br and to ap/ap. A preliminary genetic linkage map with the sex realizer F'/f and the loci br and w residing in homomorphic sex chromosomes is established. Evidence is presented that crossing over is absent in the male sex. The possible causes of the spontaneous appearance of mosaics for eye colour observed among individuals heterozygous for recessive genes are discussed.

Animals↗
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↗
PubMed2005

Extension of the SIMLA package for generating pedigrees with complex inheritance patterns: environmental covariates, gene-gene and gene-environment interaction.

We have previously distributed a software package, SIMLA (SIMulation of Linkage and Association), which can be used to generate disease phenotype and marker genotype data in three-generational pedigrees of user-specified structure. To our knowledge, SIMLA is the only publicly available program that can simulate variable levels of both linkage (recombination) and linkage disequilibrium (LD) between marker and disease loci in general pedigrees. While the previous SIMLA version provided flexibility in choosing many parameters relevant for linkage and association mapping of complex human diseases, it did not allow for the segregation of more than one disease locus in a given pedigree and did not incorporate environmental covariates possibly interacting with disease susceptibility genes. Here, we present an extension of the simulation algorithm characterized by a much more general penetrance function, which allows for the joint action of up to two genes and up to two environmental covariates in the simulated pedigrees, with all possible multiplicative interaction effects between them. This makes the program even more useful for comparing the performance of different linkage and association analysis methods applied to complex human phenotypes. SIMLA can assist investigators in planning and designing a variety of linkage and association studies, and can help interpret results of real data analyses by comparing them to results obtained under a user-controlled data generation mechanism.A free download of the SIMLA package is available at http://wwwchg.duhs.duke.edu/software.

Journal Article↗