Heterozygote advantage is the superior fitness often seen in hybrids, the cross between two dissimilar parents. A heterozygote is an organism with two different alleles, one donated from each parent. Fitness means the ability to survive and have offspring. Heterozygote advantage also refers more narrowly to superior fitness of an organism that is heterozygous for a particular gene, usually one governing a disease.. Inbreeding is the practice of repeatedly crossing a single variety of organism with itself, in order to develop a more uniform variety. During this process, the organism becomes homozygous for many genes, meaning that its two gene copies are identical. This is often accompanied by loss of vigor: slower growth, less resistance to disease, and other signs of decreased fitness. This is known as inbreeding depression. Breeding with another variety (outcrossing) produces offspring that are heterozygous for many genes, and is often accompanied by an increase in size and vigor. This ...
Looking for heterozygosis? Find out information about heterozygosis. the state, inherent in every hybrid organism, in which homologous chromosomes carry different forms of a given gene or differ in the arrangement of genes... Explanation of heterozygosis
Double heterozygosity (DH) for BRCA1 and BRCA2mutations is a very rare finding, particularly in non-Ashkenazi individuals, and only a few cases have been reported to date. In addition, little is...
β1,4-GalT1 is type II membrane-bound glycoprotein transferring galactose to acceptor sugars. This enzyme catalyzes the synthesis of lactose or transfers galactose to the terminal GlcNAc of complex-type N-glycans. Previous studies found that β1,4-GalT1 knock-out mouse showed semi-lethality after birth. We obtained a β1,4-GalT1 site-specific mutant mouse modelusing CRISPR/Cas9 in which tyrosine (Y286) were substituted by leucine (L286). This mutation makes β1,4-GalT1 an N-acetylgalactosaminetransferase instead of galactosyltransferase. No lethal deficiency was observed in both heterozygote (+/-) mice and homozygous (-/-) mice. However, homozygous (-/-) mice were unable to give birth and lactation. The further N-glycan profiling showed that homozygous (-/-) mouse serum have no sialylated N-glycans while heterozygote(+/-) mouse showed the similar pattern of N-glycosylation in serum compared with wild-type mouse. The results indicated that the functional changing of galactosyltransferase in ...
I am having trouble with this type of setup not sure about how to set up Punnett square to answer questions concerning homozygous vs.
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A communications apparatus is adapted for use with a mains electricity transmission and/or distribution network. The communications apparatus includes a signal transmission and/or reception means, and frequency conversion means for converting the frequency of a signal transmitted or received by the signal transmission and/or reception means to a frequency which facilitates improved propagation of the signal on the network. Preferably the signal transmission and/or reception means is adapted to operate according to a telephony standard with uses a relatively high carrier frequency (e.g. CT2), and the frequency conversion means is usable to covert a signal having a relatively high carrier frequency (e.g. CT2) and the frequency conversion means is usable to convert a signal having a relatively high carrier frequency to a signal having a lower carrier frequency.
2 = 59.0, with 1 d.f. given by number of phenotypes minus number of alleles). Thus, after the frost a higher proportion of individuals possessing the heterozygous condition survive than predicted by the Hardy-Weinberg formula, and both homozygotes have lower than expected survival: the moth population can be said to have undergone a small amount of evolution. If there is no evolutionary change in subsequent generations, and random mating, then the allele frequencies of 0.771 (A) and 0.229 (a) will be maintained, establishing new genotype frequencies of 0.594:0.353:0.053. Where a trait is dominant, allelic frequencies cannot be calculated from the genotypic classes because the homozygous dominants cannot be differentiated from the heterozygotes. But for such traits, or for example a disease that is expressed only in the homozygous recessive state, assuming Hardy-Weinberg equilibrium makes it possible to calculate the proportion of a population that is heterozygous. If the genetic disease is ...
rs5984894 is a SNP located within an intron of the protocadherin 11 PCDH11X gene, on the X chromosome. A study of 2,391 patients with late-onset Alzheimers disease reports that rs5984894 is particularly associated with increased risk for the disease in females, as compared to males. In this study, the patients were Americans of European descent, and 62% were female. Odds ratios were 1.75 (CI: 1.42-2.16) for female homozygotes (p = 2 x 10e-7) and 1.26 (CI: 1.05-1.51) for female heterozygotes (p = 0.01) compared to rs5984894(G;G) females.[PMID 19136949 ...
Before you begin to write, you should objectively analyze the data collected by the whole course (combined 5 lab sections). You learned from the phenotype of the heterozygous male progeny (from the cross between N2 wild type males and the Dpy Unc hermaphrodites) which strain has the x-linked mutation. Do the data from the scoring, support that conclusion that the mutations are unlinked in this strain? Note that the expected 9:3:3:1 ratio of F2 progeny of the dihybrid selfing in this strain isnt perfect. Does that mean that the two genes responsible for the two phenotypic defects arent really on different chromosomes? Do these data better support linkage? You could do a statistical test for goodness of fit (such as a Chi square) to see if it is likely that the differences between what we observed and what we expected are due to chance and, if so, that we can accept our conclusion with more confidence. Unfortunately, the Chi square test is used with a specific kind of cross that we didnt do, so ...
A diagnosis of GD has implications for other family members and family planning. Therefore, it is important to speak with a genetic counsellor who can help you make decisions about further testing.[10][11]. Mentioned above, GD is inherited in an autosomal recessive fashion, meaning that if a couple has a child with GD, it is almost always the case that they are both unaffected carriers. This means that they both have a gene change in one copy the GBA gene, and the other copy is functional. At conception, siblings of a person with GD have a 25% chance of also being affected with GD, 50% chance that they are carriers like their parents, and a 25% chance of being unaffected and non-carriers. After birth, if it is determined that the sibling is unaffected, then there is a 2/3 chance that he/she is a carrier. If a person with GD has children, then all of his/her children will be carriers ...
There are a number of genetic disease for which persons of Jewish heritage (at least one grandparent) are more likely to be carriers of than the general population. Carriers are healthy individuals, unaffected by the disease for which they carry. If both parents are carriers of a gene mutation for the same condition, there is a 25% chance, with each pregnancy, of having an affected child. These diseases are all serious and can be fatal and or life altering to children born with them ...
Das ABCA1-Gen ist ein membranständiges Transportprotein, welches insbesondere für den Cholesterintransport zuständig ist. Mutationen zeigen eine codominante Vererbung. Während heterozygote Anlageträger deutlich erniedrigte HDL-Werte aufweisen und damit ein deutlich erhöhtes Coronarrisiko besitzen, erkranken homozygote oder compound heterozygote Anlageträger an einer Tangier-Erkrankung.. ...
Aims: To assess efficacy and safety of HMG-CoA reductase inhibitor (statin) treatment in children and adolescents with heterozygous familial hypercholesterolaemia. Methods: MEDLINE, EMBASE, COCHRANE and Current Controlled Trials databases were searched. Study design, efficacy, and safety outcome-measures were extracted. Results of parallel-group randomised placebo controlled trials with low density (LDL) and high density lipoprotein cholesterol (HDL), and triglycerides as outcomes were pooled using standard meta-analytical methods. Results: One hundred and fifty seven of 1060 identified papers studied familial hypercholesterolaemia, and 18 papers reported 7 prospective case series, 1 non-randomised trial, 2 trials with active treatment control groups, and 8 parallel-group randomised placebo controlled trials (RCT). The RCTs randomised 947 children, aged 8-18 years, for periods of 6-96 weeks with an estimated 850 person-years follow-up. There were no differences in clinical or laboratory adverse
OBJECTIVES: Individuals with heterozygous familial hypercholesterolaemia (FH) are at high risk of developing cardiovascular disease (CVD). This risk can be substantially reduced with lifelong pharmacological and lifestyle treatment; however, research suggests adherence is poor. We synthesised the qualitative research to identify enablers and barriers to treatment adherence.. DESIGN: This study conducted a thematic synthesis of qualitative studies.. DATA SOURCES: MEDLINE, Embase, PsycINFO via OVID, Cochrane library and CINAHL databases and grey literature sources were searched through September 2018.. ELIGIBILITY CRITERIA: We included studies conducted in individuals with FH, and their family members, which reported primary qualitative data regarding their experiences of and beliefs about their condition and its treatment.. DATA EXTRACTION AND SYNTHESIS: Quality assessment was undertaken using the Critical Appraisal Skills Programme for qualitative studies. A thematic synthesis was conducted to ...
Succinate-CoA ligase is a heterodimer enzyme composed of Suclg1 -alpha- and a substrate-specific Sucla2 or Suclg2 -beta- subunit yielding ATP or GTP, respectively. In humans, the deficiency of this enzyme leads to encephalomyopathy with, or without methylmalonyl aciduria, in addition to resulting in mitochondrial DNA depletion. We generated mice lacking either one Sucla2 or Suclg2 allele. Sucla2 heterozygote mice exhibited tissue- and age-dependent decreases in Sucla2 expression associated with decreases in ATP-forming activity, but rebound increases in cardiac Suclg2 expression and GTP-forming activity. Bioenergetic parameters including substrate-level phosphorylation were not different between wild type and Sucla2 heterozygote mice unless a submaximal pharmacological inhibition of succinate-CoA ligase was concomitantly present. mtDNA contents were moderately decreased, but blood carnitine esters were significantly elevated. Suclg2 heterozygote mice exhibited decreases in Suclg2 expression but ...
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Alirocumab was found to be both safe and effective in reducing LDL-C in patients with heterozygous familial hypercholesterolemia.
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Familial hypercholesterolemia (FH), characterized by markedly increased low-density lipoprotein (LDL) cholesterol concentrations, is a hereditary disorder of LDL-cholesterol metabolism. The condition is common as it affects 1 in 250 persons (1-3). The ...
Generation of mice. The generation of En-1lki (lacZ knock-in) embryonic stem (ES) cells and chimeric mice in which the bacterial gene coding for β-galactosidase (β-gal), lacZ, is inserted into theEn-1 locus has been described previously (Hanks et al., 1995). Using En-1 lki/+-targeted ES cells, we generated mouse lines using two independently targeted cell lines. Male chimeras were made using morula aggregation as described byNagy et al. (1993) and bred with CD1 females (Charles River Laboratories, Wilmington, MA) to transmit the allele through the germline.. Homozygote En-1 lki/lki embryos were obtained by intercrossing heterozygote mice at F2-F6 generations. The lines were maintained on an outbred CD1 background. En-1 lki/lki embryos were morphologically indistinguishable from En-1 hd/hd (homeodomain deletion) null mutant mice (Wurst et al., 1994) and were identified by genotyping using yolk sac DNA or by morphological criteria as described previously (Wurst et al., 1994). To obtain En-1 ...
I would like to know about the level of gene expression in homozygote and heterozygote with respect to a transgenic loci and a wild type loci? I am under the impression that the level of gene expression in a homozygote and a heterozygote in the case of a dominant charcter is the same. Would somebody calrify me? Thanks, SATHYA ...
Heterozygote mice from a hybrid cross of C57BL/6J and FVB/NJ had heightened EtOH consumption, preference or blood EtOH concentration compared to either homozygous groups. The magnitude of dominant deviation on Chr. 11, as noted in Fig. 9, was measured after a drinking in the dark paradigm, 24hr two-bottle-choice and subsequent blood ethanol concentration measurement ...
Heterozygous male rictor+/- mice display a significantly decrease in median lifespan (40%) compared to wild-type controls. Liver- specific deletion of Rictor in male mice also resulted in a 30% decrease in median lifespan. In both models, the decrease in lifespan was associated by a decrease in the incidence of cancer. Inducibly deleting Rictor throughout the body in adult animals, results in a stronger phenotype with a median survival of less than 1 year. No significant changes were observed for female lifespan in any of the three models ...
rs10260404, a SNP in the region of the DPP6 gene on chromosome 7, has been associated with the sporadic form of ALS (Lou Gehrigs disease) in a study of 1000+ European patients. The overall odds ratio for the risk allele rs10260404(C) is 1.30 (CI: 1.18-1.43, p=0.017). When broken down by genotype, the odds ratios for heterozygotes are 1.20 (CI: 1.06-1.41), and for rs10260404(C;C) homozygotes, 1.60 (CI: 1.32-1.92).[PMID 18084291] A "C-C" haplotype for this SNP and that of its neighbor rs10239794 is also highly (statistically; p=10e-9) associated with ALS. [PMID 18084291] However, in an expanded study pooling 4 populations (Irish, Dutch, US, Polish) rs10260404 failed to reach Bonferroni significance. although it did remain significant in the (expanded) Irish-only population.[PMID 18987618 ...
In general, gene expression (in terms of mRNA production) should be proportional to the number of copies of the gene present in the genome. If multiple alleles of a gene are present, the expression of each should be similar. So for a gene with 2 alleles (call them A and a), the level of expression in an animal homozygous for A would be 2(A) (since it has 2 copies of the allele, assuming it got one from the father and one from the mother). A heterozygote would show levels of expression of 1(A) + 1(a), and a homozygote for a would be 2(a). This should hold true for genes introduced by transgenic methods as well, assuming that your transgene is present in similar numbers as the complementary endogenous gene, and that it did not insert into a genomic location that somehow inhibits it from being expressed. Keep in mind that this is a rather idealized explanation and there are a number of things that are not taken into account. If, for example, the function of the product of gene A is to stimulate ...
In article ,6lual9$kbc$1 at nnrp1.dejanews.com,, ramanp at my-dejanews.com wrote: , Germline gene therapy is an important area of genetic engineering... [SNIP] Wouldnt it be wonderful to be able to prune some , unwanted deadly genes from our family trees forever? I would greatly , appreciate any thoughts, suggestions or comments that anybody might have on , this serious issue. Thanks, , Priya Raman , I guess the major problem that I have with germ line therapy is that it assumes we know what we are doing; it assumes we know all the activities of a particular gene/protein. The best example is sickle cell anemia. This can be a devasting disease in homozygotes. But heterozygotes are resistant to malaria. Does that make the sickle cell allele bad or good. Depends on the environment; probably depends on other genes. Can we safely say that there are unwanted genes or do we simply not know enough about the function of these unwanted alleles? I think the major problem with germ line therapy is our ...
J:70364 Kalinichenko VV, Lim L, Stolz DB, Shin B, Rausa FM, Clark J, Whitsett JA, Watkins SC, Costa RH, Defects in pulmonary vasculature and perinatal lung hemorrhage in mice heterozygous null for the Forkhead Box f1 transcription factor. Dev Biol. 2001 Jul 15;235(2):489-506 ...
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Hello, I found that GenotypeGVCFs in GVCF mode can lead to an unexpected homozygous or heterozygous genotypes when one SNP is called within an indel.
An anonymous reader writes Nokia is worried that networks may reject selling the N900 because it wont allow them to mess with the operating system. Nokia has previously showed the N900 running a root shell and it appears to use the same interface for IM and phone functions. Meanwhile, Verizon is...
Every time new stock is obtained there is the chance of introducing pests or diseases to an existing flock, or to infect the new fowls with diseases already present. It may be the end of an heritage flock.. Birds vaccinated against a certain disease will not show the disease, but can transmit the organism and infect non-vaccinated fowls nevertheless.. Survivors of some diseases are carriers of the disease organism for life and can infect other birds.. Keeping more birds than can be comfortably housed is a good recipe for disaster.. ...
With a high probability more African primates than shown in Table 1 are carriers of an SIV, since for some species only a limited number of individuals
Immunohistochemical images of VE-cadherin at 5 and 20 weeks of age. (A) 5W of heterozygotes, (B) 5W of homozygotes, (C) 20W of heterozygotes, (D) 20W of homozyg
Ramos EM, Carecchio M, Lemos R, Ferreira J, Legati A, Sears RL, Hsu SC, Panteghini C, Magistrelli L, Salsano E, Esposito S, Taroni F, Richard AC, Tranchant C, Anheim M, Ayrignac X, Goizet C, Vidailhet M, Maltete D, Wallon D, Frebourg T, Pimentel L, Geschwind DH, Vanakker O, Galasko D, Fogel BL, Innes AM, Ross A, Dobyns WB, Alcantara D, ODriscoll M, Hannequin D, Campion D. Primary brain calcification: an international study reporting novel variants and associated phenotypes. Eur J Hum Genet. 2018 10; 26(10):1462-1477 ...
Glucose-6-phosphate dehydrogenase (G6PD) deficiency, the most common enzymopathy of humans, affects over 400 million people. The geographical correlation of its distribution with the historical endemicity of malaria suggests that this disorder has risen in frequency through natural selection by malaria. However, attempts to confirm that G6PD deficiency is protective in case-control studies of malaria have yielded conflicting results. Hence, for this X-linked disorder, it is unclear whether both male hemizygotes and female heterozygotes are protected or, as frequently suggested, only females. Furthermore, how much protection may be afforded is unknown. Here we report that, in two large case-control studies of over 2,000 African children, the common African form of G6PD deficiency (G6PD A-) is associated with a 46-58% reduction in risk of severe malaria for both female heterozygotes and male hemizygotes. A mathematical model incorporating the measured selective advantage against malaria suggests that a
Matrix Metalloproteinase-2 (Mmp2) is a collagenase known to be important in the development of renal fibrosis. In unilateral ureteral obstruction (UUO) the obstructed kidney (OK) develops fibrosis, while the contralateral (CL) does not. In this study we investigated the effect of UUO on gene expression, fibrosis and pelvic remodeling in the kidneys of Mmp2 deficient mice (Mmp2-/-), heterozygous animals (Mmp2+/-) and wild-type mice (Mmp2+/+). Sham operated animals served as controls (Cntrl). UUO was prepared under isoflurane anaesthesia, and the animals were sacrificed after one week. UUO caused hydronephrosis, dilation of renal tubules, loss of parenchymal thickness, and fibrosis. Damage was most severe in Mmp2+/+ mice, while both Mmp2-/- and Mmp2+/- groups showed considerably milder hydronephrosis, no tubular necrosis, and less tubular dilation. Picrosirius red quantification of fibrous collagen showed 1.63±0.25% positivity in OK and 0.29±0.11% in CL (p,0.05) of Mmp2+/+, Mmp2-/- OK and ...
The foregoing examples show that the finding of population heterozygote advantage, as in the infectious disease studies cited, does not support an inference of allele-specific overdominance, the condition of primary interest as an immunological hypothesis and a mechanism for the maintenance of MHC diversity. Put another way, population heterozygote advantage may appear due to a combination of the two distinct mechanisms we defined in the Introduction: the protective or detrimental effects of particular alleles (R and S alleles in our model), and the effects of heterozygosity itself. The effects of R and S alleles appear as effects of heterozygosity vs. homozygosity because heterozygotes and homozygotes will in general carry different distributions of S and R alleles; thus, in an analysis that fails to condition on the alleles carried, heterozygosity is confounded with the alleles carried.. One advantage of correctly separating the effects of individual alleles from the effects of heterozygosity ...
A carrier frequency modulating system and method for producing a modulated carrier frequency is disclosed. The system comprises a carrier frequency signal generator for producing a carrier frequency signal at a carrier frequency at an output thereof. The system further comprises a sequencer for producing a modulation signal at an output thereof. This modulation signal comprises a plurality of modulation signal portions separated by at least one null modulation signal portion having a corresponding time length. The system is provided with a modulator for producing a modulated carrier frequency signal at an output thereof. The modulator has a first input connected to the output of the carrier frequency signal generator for receiving the carrier frequency signal, and has a second input for receiving the modulation signal. The system further comprises a power supply unit for supplying electrical power to the carrier frequency signal generator. The sequencer is connected to the carrier frequency signal
In heterozygote advantage, or heterotic balancing selection, an individual who is heterozygous at a particular gene locus has a greater fitness than a homozygous individual. Polymorphisms maintained by this mechanism are balanced polymorphisms.[3] Due to unexpected high frequencies of heterozygotes, and an elevated level of heterozygote fitness, heterozygotic advantage may also be called "overdominance" in some literature. A well-studied case is that of sickle cell anemia in humans, a hereditary disease that damages red blood cells. Sickle cell anemia is caused by the inheritance of an allele (HgbS) of the hemoglobin gene from both parents. In such individuals, the hemoglobin in red blood cells is extremely sensitive to oxygen deprivation, which results in shorter life expectancy. A person who inherits the sickle cell gene from one parent and a normal hemoglobin allele (HgbA) from the other, has a normal life expectancy. However, these heterozygote individuals, known as carriers of the sickle ...
Several previous studies have examined the role of muscle glucose transport in whole body glucose homeostasis using genetically engineered mice with whole body GLUT4 disruption and have shown conflicting results (19-22). Katz and colleagues (19) have shown that mice with homozygous disruption of whole body GLUT4 have normal fasting plasma glucose and insulin concentrations (at 2-4 months of age). Similarly, Rossetti and colleagues (20) have shown that mice with heterozygous disruption of whole body GLUT4 (at 4-5 months of age) have normal plasma glucose concentration despite a significant decrease in insulin-stimulated muscle glucose transport. In contrast, Stenbit and colleagues (21) found that mice with heterozygous disruption of whole body GLUT4 develop a diabetes phenotype (e.g., hyperglycemia) associated with decreases in insulin-stimulated glucose transport in skeletal muscle. The reason for this discrepancy is unclear but may be due to a difference in the age of mice. In this regard, ...
Anxiety is often comorbid with depression (Zimmerman et al., 2002). In rodents, some animal models of "depression" display anxiety-like responses (Bale et al., 2000; Schramm et al., 2001; Ansorge et al., 2004; Heim et al., 2004; Wei et al., 2004), whereas others do not (Overstreet, 1993). To determine whether Vmat2 mice show anxiety-like behaviors, animals were subjected to the open field, zero maze, light-dark exploration, and novelty-suppressed feeding tests. Because behaviors of WT and Vmat2 heterozygotes were indistinguishable among these tests, these findings suggest anxiety is not a comorbid feature of the VMAT2 phenotype. Interestingly, these results are similar to those for reserpine-treated hypertensive patients, where anxiety does not appear to accompany their depressive-like states (Freis, 1954).. A core symptom of depression is anhedonia (American Psychiatric Association, 1994). This behavior is modeled as an endophenotype in Flinders rats, learned helpless mice, the chronic mild ...
The Genetics Society of America (GSA), founded in 1931, is the professional membership organization for scientific researchers and educators in the field of genetics. Our members work to advance knowledge in the basic mechanisms of inheritance, from the molecular to the population level.. Online ISSN: 1943-2631. ...
Choosing to participate in a study is an important personal decision. Talk with your doctor and family members or friends about deciding to join a study. To learn more about this study, you or your doctor may contact the study research staff using the contacts provided below. For general information, Learn About Clinical Studies. ...
PubMed comprises more than 30 million citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.
Type: JAX GEMM Strain - Mutant Strain Ty … Type: JAX GEMM Strain - Mutant Strain Type: JAX GEMM Strain - Spontaneous Mutation TJL Mating System: Outcross-Intercross (Female x Male) TJL Breeding Summary: homozygote x B6CBACa-Aw-J/A F1 then obligate heterozygote x heterozygote Species: laboratory mouse Generation: N68F1 (07-NOV-05) Appearance white-bellied agouti, ataxic Related Genotype: Aw-J/? Kcnj6wv/Kncj6wv OR agouti, ataxic Related Genotype: A/A Kcnj6wv/Kncj6wv OR white-bellied agouti, unaffected Related Genotype: Aw-J/? +/? or Aw-J/A Kncj6wv/+ OR agouti, unaffected Related Genotype: A/A +/? or A/A Kncj6wv/+ Strain Description Mice homozygous for the weaver spontaneous mutation (Kcnj6wv) are recognizable in the second postnatal week by their small size, instability of gait, weakness, and hypotonia. Many homozygous mutant mice die at weaning age, but some survive to adulthood, and females may breed. The cerebellum in homozygous mutants is very small, simple, and almost devoid of granule ...
The t-haplotype is a chromosomal region in Mus musculus characterized by meiotic drive such that heterozygous males transmit t-bearing chromosomes to roughly 90% of their offspring. Most naturally occurring t-haplotypes express a recessive embryonic lethality, preventing fixation of the t-haplotype. Surprisingly, the t-haplotype occurs in nature as a persistent, low-frequency polymorphism. Early modeling studies led LEWONTIN to hypothesize that this low level polymorphism results from a balance between genetic drift in small demes and interdemic migration. Here, we show that while combination of deme size and migration rate that predict natural t-haplotype frequencies exist, the range of such values is too narrow to be biologically plausible, suggesting that small deme size and interdemic migration alone do not explain the observed t-haplotype frequencies. In response, we tested other factors that might explain the observed t-polymorphism. Two led to biologically plausible models: substantially reduced
definition of heterozygote - (genetics) an organism having two different alleles of a particular gene and so giving rise to varying offspring
Recurrence relations are derived for the natural selection of a selective coefficient that is subject to additive genetic variations. Mathematical models are set up of the natural selection of the selective coefficient of the heterozygote. A general computer model of genetical populations is described and populations are set up to simulate genetic variation of the heterozygote. The theoretical models are applied to the spread of a gene under natural selection. If the heterozygote is initially intermediate between the two homozygotes, the evolution of semi-dominance, dominance or over-dominance depends on the genetic variance in fitness. Over-dominance evolves if the standard deviation in fitness due to genetic causes is about 0.7 times the difference between the initial heterozygote and homozygote fitnesses. The heterozygote will then continue to increase in fitness until the characters that determine the fitness are at their optimum values. Thus the polymorphism tends to become more stable. The ...