Entirely new genetic trait emergence with homologous chromosomes, how?
153580
there are nonsense parts in our DNA called transposable elements, they can move around our DNA on their own and insert themselves into genes and promoters drastically changeing there function
538795
Yeah...that's not possible.\n\nDon't get me wrong, it's theoretically possible.  But our technology is nowhere near sophisticated enough to even identify the genetic basis of most traits (except for specific genetic diseases and the simplest traits like hair color) let alone manipulate them.  Also, very few of what we call "traits" when we are talking about humans, have a genetic basis.  Genes have various amounts of influence on them but you can't simply alter a few genes and change them.\n\nWe do this all the time with lower organsims like plants and bacteria. For example, something not widely known is that roughly 50% of all lard actually comes from plants that have had the genes for animal fats implanted into them.  At least in the US, the law specifically allows this to be used without being labeled as such and almost all commercial lard is roughly 50% real lard and 50% vegetable based lard mixed together.\n\nPeople ain't plants, however.  Genes for us are fiendishly complex where in plants, they are simple.  Other than cloning, I don't see any form of gene manipulation technology being successful anytime soon.
997040
Eye color is a polyploid trait.  the actual genes occur on a couple of different chromosomes.  Sorry.  The human genome project has it mapped out which chromosomes they are my poster is at work.
264396
Great stuff going on right now having to do with developmental genes (like Hox genes).  You may know this as "Evo Devo" or evolutionary developmental biology.\n\nCheck out the book "Endless Forms Most Beautiful," by Sean Carroll.  He also gives ideas for research and new fields, lots of peer-reviewed papers.\n\nI just read it this Fall, it was great.
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
96132
There have been hundreds of thousands of such experiments done. Moreover you can easily do them yourself using some nutriemt agar and an incubator with a few hundred dollars to pay someone to do the genetic workup.\n\ntalk.origins is your one stop shop for these types of quetsions. The site is highly reputable, well refernces, cites peer reveiewed science journals and most importantly lists literally hundreds of experimenst that show exactly what you describe.\n\nI've attached a couple link to pages that list a dozenor so such mutation studies, but the site has many hundreds of others.
400289
The only artificial chromosome I have heard about was created for yeast cells.  They are eukaryotic (vs. prokaryotic bacteria) thus they have (4?) chromosomes like us.  I don't know exactly how they made it, but I think they just introduced another altered copy of one of their natural chromosomes that they would tolerate.  They also made it so they could put whatever genes of interest into the chromosome for further studies.
961718
In population genetics, the Hardy–Weinberg principle (HWP) (also Hardy–Weinberg equilibrium (HWE), or Hardy–Weinberg law), named after G. H. Hardy and Wilhelm Weinberg, states that, under certain conditions, after one generation of random mating, the genotype frequencies at a single gene locus will become fixed at a particular equilibrium value. It also specifies that those equilibrium frequencies can be represented as a simple function of the allele frequencies at that locus.\n\nIn the simplest case of a single locus with two alleles A and a with allele frequencies of p and q, respectively, the HWP predicts that the genotypic frequencies for the AA homozygote to be p2, the Aa heterozygote to be 2pq and the other aa homozygote to be q2. The Hardy–Weinberg principle is an expression of the notion of a population in "genetic equilibrium" and is a basic principle of population genetics.\n\nThe original assumptions for Hardy–Weinberg equilibrium (HWE) were that the organism under consideration is:\n\nDiploid, and the trait under consideration is not on a chromosome that has different copy numbers for different sexes, such as the X chromosome in humans (i.e., the trait is autosomal) \nSexually reproducing, either monoecious or dioecious \nDiscrete generations \nIn addition, the population under consideration is idealised, that is:\n\nRandom mating within a single population \nInfinite population size (or sufficiently large so as to minimize the effect of genetic drift) \nand experiences:\n\nNo selection \nNo mutation \nNo migration (gene flow) \nThe first group of assumptions are required for the mathematics involved. It is relatively easy to expand the definition of HWE to include modifications of these, such as for sex-linked traits. The other assumptions are inherent in the Hardy-Weinberg principle.\n\nA Hardy-Weinberg population is used as a reference population when discussing various factors. It is not surprising that these populations are static.
1181866
there are databases with which you can do homology searches. best to know what genes you are looking for though as genome wide homology may be difficult to search for\ntry the ensemble database:\nhttp://www.ensembl.org/index.html\notherwise a broad literature search might be better suited. odds are someone else has already done a similar comparison.\n\nfound this old review\n\nhttp://www.sciencedirect.com/science?_ob=MImg&_imagekey=B6VS0-45765F9-2J-1&_cdi=6248&_user=911953&_orig=search&_coverDate=06%2F30%2F1997&_qd=1&_sk=999929996&view=c&wchp=dGLbVtz-zSkWA&md5=03f894feac6d92afb553850237f34bcf&ie=/sdarticle.pdf\n\nmight be of some help. if the link doesnt work, can be found using a Pubmed search.
708035
I can only answer number one.\nThe possible traits can be determined.  But there's no way of know the exact traits of the offspring unless the parents have either two dominate or two recessive genes with every specif trait.  For instance, using punnett square:\n \n----d----d\nD  Dd Dd\nD  Dd Dd\n\nAll the possible genotypes are the same.\nSorry I couldn't answer your other questions!
64866
The offspring of two humans is human. Until scientists declare that there is a homo superior intead of a homo sapien based on chromosome differences, there can be no other result.
425063
2 recessive alleles - Homozygotes
598234
a group of lines that are genetically identical except at one or a few loci.
841943
Mendel's laws predict that a monohybrid cross between any two heterozygotes would produce offspring in a 3:1 phenotypic ratio.  That is:\nAa  X  Aa = \n1 AA - Dominant Phenotype\n2 Aa - Dominant Phenotype\n1 aa - Recessive Phenotype\n\nSo, 3 Dominant : 1 Recessive\n\nNow for your two instances:\n\nA.\nIn the case of codominance we have two different dominant alleles and one recessive allele.  When both dominant alleles are present, the phenotype is different from that seen when either of the alleles is present alone (homozygous or heterozygous).  A classic example of codominance is that of blood types.  Type A and type B are both dominant phenotypes, type O is the recessive phenotype, and type AB is the codominant phenotype.\n\nBack to your question, lets say:\nA = dominant allele 1\nA* = dominant allele 2\na = recessive allele\n\nCrossing two heterozygotes: Aa X A*a results in\n1 AA* - codominant phenotype\n1 Aa - dominant allele 1 phenotype\n1 A*a - dominant allele 2 phenotype\n1 aa - recessive phenotype\n\nSo we have a 1:1:1:1 phenotype ratio, not Mendelian expected 3:1\n\nB.\nRecessive lethal alleles are a situation where the homozygous recessive genotype is lethal to the organism.  So if we cross two heterozygotes:\n\nAa X Aa \n\nWe get:\n\n1 AA - dominant phenotype\n2 Aa - dominant phenotype\n1 aa - lethal, so this offspring is never seen\n\nSo here all the offspring seen are of the dominant phenotype, again defying Mendel's predicted 3:1 ratio.\n\nHope this helps!
219241
Scientists have reported that they've found an "extremely unusual" trait in the cells of some mothers with two or more gay sons, providing more evidence to suggest that homosexuality might be inherited.\n\n\nMothers of multiple gay sons were about six times more likely than other women to process their X chromosomes in a certain way, researchers discovered.\n\n\nResearchers aren't entirely sure what the findings mean, said study co-author Sven Bocklandt, a postdoctoral researcher at UCLA. Making things more complicated, about 75 percent of mothers of multiple gay sons don't have the trait.\n\n\nStill, the study, released Tuesday in the journal Human Genetics, raises plenty of questions, Bocklandt said, especially as researchers try to figure out whether homosexuality has genetic roots and if there truly is a "gay gene" -- or genes.\n\n\n"What everybody wants is the gene, and we don’t have it yet," Bocklandt said. "But this is an independent confirmation that the X chromosome is involved."\n\n\nBocklandt and colleagues looked at a phenomenon known as X-chromosome inactivation, in which cells inside the bodies of females automatically turn off -- or inactivate -- one of their two X chromosomes. That leaves them with one working X chromosome -- just like males, who have a single X and a single Y chromosome.\n\n\nNormally, each cell in a female's body randomly turns off one or the other X chromosome. In some cases, such as when families share a genetic disease, there is "extreme skewing" -- one X chromosome is more likely to be turned off than the other, Bocklandt said.\n\n\nIn the new study, the researchers looked at 97 mothers of one or more gay sons and 103 women with no gay sons to see what their blood cells did with their X chromosomes. The researchers recruited many of the women with the help of PFLAG.\n\n\nThey found that nearly a quarter of the mothers of multiple gay sons inactivated the same X chromosome -- in other words, nonrandomly -- compared to just 4 percent of the women without gay sons. Of those with one gay son, 13 percent inactivated the same X chromosome.\n\n\nDr. Ionel Sandovici, a genetics researcher at the Babraham Institute in Cambridge, England, who is familiar with the research findings, cautioned that the study is small, with just 44 mothers of multiple gay sons being examined. More research in larger groups must be done to confirm the results, Sandovici said.\n\n\nThe research does provide "circumstantial evidence" that the X chromosome contributes to the development of male sexuality, Sandovici said. But "we still understand very little about molecular mechanisms of sexual orientation, and this seems to be rather a complicated biological puzzle."\n\nBut of course its Nature vs. Nurture and its possible that the person could just become gay because of his environment/experiences or just be born that way.
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.
98654
Do refer to websites, such as Wikipedia, Vivisimo or Google; you will find countless articles, links and so on. Start with any scientific term, such as 'chromosome' and it will get you somewhere. Kimballs Biology Pages are a wonderful bet too.