what is a repeat allele?
597475
> Allele is a gene concerned with one of the contrasting characters (Tall and Short).\n> The occurrence of more than two alleles in a population at the same loci in the chromosome is called multiple allele or repeat allele.
116048
same number but one is just mutated
668934
AAxAa--->1/2AA:1/2Aa\nBBxBb---->1/2BB:1/2Bb\nCCxCc--->1/2CC:1/2Cc\n====>frequency of perfect heterozygous(AaBbCc)=\n  1/2x1/2x1/2=1/8
250276
It is most definetly a recessive gfene. I know this because so few people posses this trait. However there is a possibility of it occuring. Actually the small big toe depends not just on one allele but several alleles at several loci but in the end all sucha lleles are recessive and do not give heterozygote advantage
52176
Genetic predisposition.
957887
Each chromosome in your body has an "identical pair"- there are two chromosomes that code for the same functions- one from your mother and one from your father.\n\nBecause they come from two sources, they are coding for the same functions, but may code differently for them (ie blue eyes as opposed to brown eyes).\n\nDuring prophase one, each chromosome duplicates into two sister chromatids joined by a centromere, and then the double stranded chromosome finds it's partner which is coding for the same thing (just came from the opposite parent), and is also double stranded.  Now you have a 4 stranded tetrad.\n\nGenetic variability comes from crossing over.  This is where the two chromatids closest together in the tetrad exchange some genetic information.\n\nFor example, two of the chromatids code for blue eyes, brown hair and shortsightedness.\nThe other two chromatids code for brown eyes, red hair and normal vision.\n\nDuring crossing over one chromatid from each pair forming the tetrad literally have ends "crossing over" and bits of information are exchanged.\n\nAfter crossing over, you have 4 chromatids with unique codings.  Using the example above, we may now have:\n-blue eyes, brown hair, shortsightedness\n-blue eyes, red hair, normal vision\n-brown eyes, brown hair, shortsightedness\n-brown eyes, red hair, normal vision\n\nWe now have genetic variability in each gamete produced from this meiotic division.
977731
At the four strand stage 50% of the product at meiosis would be recombinant. At the two strand stage, all the products would be recombinants. Providing that the crossover in question happens every time.\n\nWithout knowing the location of the gene and which chromosome it is on then it is impossible to tell how many map units are affected.
836450
The reason repetitive sequences often do not affect the carrier's phenotype is because many repetitive sequences are in what we know as "introns" or unexpressed regions of DNA. While our DNA contains an enormous amount of data, often only a small sequence of nucleotides is necessary to make the proteins that produce a phenotype. These active sequences are in expressed portions of the DNA, or "exons." In addition, sometimes a single strand of DNA carries sequences for many different types of characteristics in an individual, but have different portions of the DNA expressed. Therefore, what may be an intron for, say, eye color, may be an exon for hair color.
797469
Your genotype determines your blood type before your born. There are three alleles or versions of the blood type gene: A, B, and O. Since everybody has two copies of these genes, there are six possible combinations; AA, BB, OO, AB, AO, and BO. In addition to the proteins (agglutinogens) existing on your red blood cells, other genes make proteins called agglutinins (a-GLOO-tin-ins) that circulate in your blood plasma. Agglutinins are responsible for ensuring that only the blood cells of your blood type exist in your body. People who have an AA genotype are said to have type A blood because the agglutinogen on their red blood cells has the enzyme activity associated with the A allele. It is important to recognize that people with the AO genotype also have the enzyme activity associated with the A allele, so they are also said to have type A blood. People with the BB and the BO genotypes are said to have type B blood. People who have the AB genotype have the enzyme activity associated with both the A and B alleles. These people have no agglutinins in their blood plasma.  In the case of blood type, both the AA and AO genotypes cause individuals to display the A blood type phenotype. Similarly, both the BB and BO genotypes cause individuals to display the B blood type phenotype. Individuals who are phenotypically type O or type AB have only one possible genotype, OO and AB, respectively. In different parts of the world, the fraction of individuals with blood type A, B, O, or AB differs. The frequency with which blood types are observed is determined by the frequency with which the three alleles of the ABO gene are found in different parts of the world (allele frequency). Variation in the allele frequency at the ABO gene reflects the social tendency of populations to marry and reproduce within a national, regional, or ethnic group. As people throughout the world intermingle to a greater extent, the distribution of the different blood types will become more uniform throughout the world. Hopefully that helps a bit!
230841
Hi. First off, its "deScent with modification".\nThat was Darwin's term for what is now known as genetic variability in a population, and a stage of his proposed evolutionary mechanism, natural selection.\nHe did not have the genetic background to explain the variations that he saw generation after generation (Mendel's works had been ignored at the time), but he noticed that in every new generation, the individuals showed varied characteristics: some traits where similar to their parents, but others were novel or maybe similar to those of older ancestors. \nThese variations occur because of 1) spontaneous mutations in the parental gametes; 2) recombination between homologous chromosomes during gamete formation (crossing over); 3) the combination of the parents' genotypes to form the genotype of the offspring (this is not strictly new material, only a new combination of preexisting ones).\n\nOnce there is a new generation of individuals that are growing and living together, some of those characteristics may result in better adjustment to the environment. The individuals with those "adaptively advantageous" traits will have higher probabilities of growing, maturing and reproducing more, with respect to other individuals. \nIf those advantageous characteristics are heritable, that is, if they are determined by the individual's combination of alleles (=the two versions of the same gene in each of us), when the individual is able to "pass them on" to more descendants those alleles will spread in the population, and eventually be present in most individuals. This, in a nutshell, is natural selection. NS leads to gradual adjustment of the population with respect to its environment.\nFrom a population genetics perspective, evolution is defined as _the change in allele frequencies_; thus, "descent with modification", coupled with evolutionary factors, leads to evolution of the population. \nIn addition to mutation and natural selection, this change in allele frequencies may be occasioned by migration (genetic flux among different populations), genetic drift (a random process) and selective mating (which strictly speaking only alters the proportion of combinations, but does not produce new material).\n\nSorry for the lengthy answer, but evolutionary processes need a little context to be understood. Good luck with your explanation!
617602
MS is not strictly a hereditary disease. However, increasing scientific evidence suggests that genetics may play a role in determining a person's susceptibility to MS. Some populations, such as the Roma, Inuit, and Bantus, never get MS. The indigenous peoples of the Americas, the Japanese, and other Asian peoples have very low incidence rates. It is unclear whether this is due mostly to genetic or environmental factors.\n\nIn the population at large, the chance of developing MS is less than a tenth of one percent. However, if one person in a family has MS, that person's first-degree relatives—parents, children, and siblings—have a one to three percent chance of getting the disease.\n\nFor identical twins, the likelihood that the second twin may develop MS if the first twin does is about 30%; for fraternal twins (who do not inherit identical gene pools), the likelihood is closer to that for non-twin siblings, or about 4%. The fact that the rate for identical twins both developing MS is significantly less than 100% suggests that the disease is not entirely genetically controlled. Some (but definitely not all) of this effect may be due to shared exposure to something in the environment, or to the fact that some people with MS lesions remain essentially asymptomatic throughout their lives.\n\nFurther indications that more than one gene is involved in MS susceptibility comes from studies of families in which more than one member has MS. Several research teams found that people with MS inherit certain regions on individual genes more frequently than people without MS. Of particular interest is the human leukocyte antigen (HLA) or major histocompatibility complex region on chromosome 6. HLAs are genetically determined proteins that influence the immune system.\n\nThe HLA patterns of MS patients tend to be different from those of people without the disease. Investigations in northern Europe and America have detected three HLAs that are more prevalent in people with MS than in the general population. Studies of American MS patients have shown that people with MS also tend to exhibit these HLAs in combination-that is, they have more than one of the three HLAs-more frequently than the rest of the population. Furthermore, there is evidence that different combinations of the HLAs may correspond to variations in disease severity and progression.\n\nStudies of families with multiple cases of MS and research comparing genetic regions of humans to those of mice with EAE suggest that another area related to MS susceptibility may be located on chromosome 5. Other regions on chromosomes 2, 3, 7, 11, 17, 19, and X have also been identified as possibly containing genes involved in the development of MS.\n\nThese studies strengthen the theory that MS is the result of a number of factors rather than a single gene or other agent. Development of MS is likely to be influenced by the interactions of a number of genes, each of which (individually) has only a modest effect. Additional studies are needed to specifically pinpoint which genes are involved, determine their function, and learn how each gene's interactions with other genes and with the environment make an individual susceptible to MS.
1000146
Do you mean RFLPs?\n\nRestriction fragment length polymorphisms?\n\nThey are used in genetic fingerprinting.  In theory anyway, SNPs are much more numerous, and easier to genotype if you have a good platform for it.
1053947
no, because it is a defect on human chromosome 21, where 3 copies are made instead of 2. this has never been seen to occur in the genomes of other organisms.
771405
40.\nhttp://www.research.att.com/~njas/sequences/b000602.txt
359265
No, we make presumptions given known mutation rates.  For mammals it's about 1 error in 10^9 bp.  So each time a cell replicates on average there will be 3 errors.  Also population geneticists, who study variation of DNA in populations, have established a set of makers in several mammallian species including humans and mice that look at variation at specific loci which tend to be heterozygous.  These loci are called microsattellite, or minisatellites.  There are other things population geneticists use but mostly they look at specific DNA loci via PCR and gel separation techniques.  Hope this helps
883749
most recurrent strip would be red id say
492162
its true that no two person can have the same DNA...\n\nbut the determination of parental disputes is not done by matching the DNA but by matching the small sequences present on the DNA known as Genes...\n\na collection of a set of genes on DNA is called chromosome..\n\nsince a child has 50% characteristics of both the father and the mother, he has the same set up of genes in his/her chromosomes.. on the chromosomes, there are many sites which are exclusive to that set of gene and chromosome and are known as VNTR's VARIABLE NUMBER TANDEM REPEATS...\n\nthese sites are very unique, they differ from person to person but remain in the same place in a lineage.... this very property of the genes on the chromosome containing DNA accounts for the determination of parental disputes..\n\n\nfor eg:   suppose in gene A, of Chromosome 1 ur mom has 5 VNTR alternatively and ur dad had 3...\n\nso if u a guy then u'll have the same 3 VNTR's on the gene containing chromosome..\n\nas simple as that..\n\nhope u got the point...