genetics:what is a dominant negative receptor?
396590
Its more than nonfunctional.  Most receptors consist of two separate proteins that complex together upon ligand binding.  This complexing allows activation of the receptor.  Dominant negatives will somehow disturb the function of the wild-type (normal) receptor.  How this happens depends on the mutation.  It could bind the normal receptor but not allow receptor activation. The important point is that a dominant negative mutation needs only one copy of the gene to be mutated to have a physiological effect, whereas normally two mutations are required to knockout gene function.  So this promotes cancer and other things.
830750
1. heterozygous: Punnett square is Pp x pp\n2. dominant b/c if it was recessive that would be the only type of allele the parents would pass on and all their children would have to be intensely freckled\n3. the Punnett square would be a 4x4 box with the B's and C's independant of each other. so on one side you have BC, Bc, bC, and bc with all of those showing up on the other side as well b/c the female was the same genotype as the male.  Obviously the black color is dominant b'c the male is heterozygous and black so all heterozygous offspring and all homozygous dominant offspring will be black as well.  the question gets a little fuzzy here though, i think you may have left some out b/c we don't know which of the two genes controls color or if they both do how the interaction between them works.  I'd be glad to help further if you have any more information to supply.
821121
Because dominant mutations will be selected against.  Keep in mind for all dominant mutations, a phenotype will be expressed, and in a lot of these cases, the gene may not be passed on because the affected person may not be able to reproduce (or will be dead before he/she can reproduce). \n\nRecessive mutations can be carried without expressing a phenotype, so unless both alleles are mutated, no phenotype will be expressed.
484436
Without knowing the names, I can tell you what an agonist and antagonist do in general, in receptor-mediated signal transduction.  An agonist acts to mimic the natural ligand, so it activated the receptor transduction system.  An antagonist is the opposite-it binds the receptor and inhibits the signal transduction system.
449038
Dominance and recessive have nothing to do with frequency of an allele.  Basically, O is recessive because if you have an A allele and an O allele you will have type A blood, and if you have a B allele and an O allele you will have type B blood.  However, O is the most common type because most people don't have an A or a B allele, but just two O's.  The fact that A or B will be expressed if you have one doesn't make it more likely that you will have one.\n\nA and B are co-dominant (that's where the AB bloodtype comes from), but O is recessive to both A and B as it does not appear in the phenotype if an A or B allele is present.  Incidentally, these alleles are typically denoted I superscript A for A, I superscript B for B, and i for O, which reflects the dominance pattern as capital letters typically indicant dominant and lowercase indicate recessive.
16479
Mutations in chromosome 7 have been linked to asthma, and parts of the GPRA gene have been associated with asthma and certain inherited allergies.  Two genes, GPRA and AAA1, located on chromosome 7, produce a protein found on the cells of the airway and also on visceral or smooth, involuntary (automatic) muscle cells.  This protein has a direct impact on the onset of asthma, since asthma is an inflammation coupled with muscle constriction of the air passages.\n\n-Colourgirlie ^_^.
699803
There are two type of alleles: dominant and recessive.\n\nThe rule of dominance is basically that if dominant is present in the allele, the phenotype (appearance) will not show the recessive gene.\n\nIn Mendel's pea plant experiment, his dominant was purple flower  (PP) and recessive was white flower (pp). \nWhen he crossed purple with white, he got all purples, with genotype (gene) of Pp. Since purple is dominant and is present in genotype, the flower is purple.
1177562
you're asking this question because the darker-skin pigment genes *do* tend to be dominant or co-dominant. the answer may go back to your father's parentage ... were his recent ancestors all latino? recessive genes can skip generations before showing up.
842615
Your question requires more knowledge of science and genetics than I have.  However, since you haven't received much help with it I thought I would give you a couple of sites.  Try these - they may be of some help to you.  Sorry I couldn't help more.
190009
yeah like the first person says. it all depends because there are dominant and recesive genes or chromosomes or whatever, and i think green is dominant, but if you get get 2 blues they dominate over 1 green, i think that is how it works.
228927
On the plasma membrane of the red blood cell (that's what the others said, and they're right).  \n\nThere is also a gene that some people carry that code for free A and B antigens in body fluids.  These people are called secretors, and the gene is dominant.\nFor example, I am a secretor.  I have determined my blood type by adding antibodies to my saliva, as well as by traditional blood tests.
732538
1RR, 2 Rr, and 1 rr   (a genotypic ratio of 1:2:1)\n\nwe just learned this in my bio class too!\nyou can use a punnett square to solve problems like this. you can look up punnett squares online, but you would set one up with an R and an r on both sides.\n\ni hope that helps!
751833
Saead70 How are you dude! I am teacher at Case Western Reserve University in Cleveland, Ohio and this will help you\n\nWe previously produced three congenic strains carrying lupus susceptibility genes (Sle1-Sle3) from the lupus-prone NZM2410 mouse on the C57BL/6 background and characterized their component phenotypes. Sle1 mediates the loss of tolerance to nuclear antigens; Sle2 lowers the activation threshold of B cells; and Sle3 mediates a dysregulation of CD4+ T cells. We have now created a collection of bi- and tricongenic strains with these intervals and assessed the autoimmune phenotypes they elicit in various combinations. Our results indicate that Sle1 is key for the development of fatal lupus. The combination of Sle1 with Sle2, Sle3, or the BXSB-derived autoimmune accelerating gene yaa results in the development of systemic autoimmunity with variably penetrant severe glomerulonephritis culminating in kidney failure. In contrast, two locus combinations of Sle2, Sle3, and yaa failed to mediate fatal disease. These results indicate that the loss of tolerance to chromatin mediated by Sle1 is essential for disease pathogenesis and identify the pathway occupied by Sle1 as a strategic target for therapeutic intervention in systemic lupus erythematosus. The coexpression of Sle1, Sle2, and Sle3 as a B6-triple congenic results in severe systemic autoimmunity and fully penetrant, fatal glomerulonephritis. These results demonstrate the fulfillment of the genetic equivalent of Koch's postulate, where susceptibility loci in a lupus-prone strain have been identified by a genome scan, isolated and functionally characterized by congenic dissection, and finally shown to mediate full disease expression when recombined in a normal genome.\n\n \nTop \nAbstract \nMaterials and Methods \nResults \nDiscussion \nReferences   \nAlthough the effector mechanisms responsible for the clinical features of systemic lupus erythematosus (SLE) have been studied extensively (1), the primary immunological defects responsible for the initiation and progression of disease remain poorly understood. A wealth of data clearly indicates, however, that genetic predisposition is a key element in susceptibility (2, 3). Several mouse models of lupus displaying different phenotypes and genotypes have collectively contributed a great deal toward our understanding of the disease and have led to the identification of more than 20 genomic intervals associated with susceptibility to SLE or SLE-related phenotypes (4–6). In the NZB/NZW-related NZM2410 lupus-prone strain, we have specifically identified the genomic positions of three recessive loci [Sle1, Sle2, and Sle3 on chromosomes (chr) 1, 4, and 7, respectively] that are strongly associated with SLE-susceptibility (7).\n\nAlthough linkage analyses have provided valuable information about the number and locations of susceptibility genes in lupus-prone strains, they have supplied little information about the nature of the component phenotypes each locus contributes, or how they interact to produce the immunopathology characteristic of the susceptible parental strains. We have adopted a congenic dissection approach to address these issues (8). The basic principle of this approach is to convert a polygenic system into a series of monogenic systems in individual congenic strains, each carrying a single susceptibility interval on a resistant genetic background. The component phenotypes expressed in these strains are amenable to genetic and functional analysis as Mendelian traits. The selection process driving the congenic derivation is purely genetic, i.e., a specific genomic segment is transferred from one strain to another (9). We have produced three congenic strains (10), B6.NZMSle1, B6.NZMSle2, and B6.NZMSle3, by moving each susceptibility interval onto the C57BL/6 (B6) background (Table 1) and used these strains to characterize the primary phenotypes associated with the Sle loci (11). \n\nSle1 mediates the loss of
231969
The Pepper trait is dominant over the melanic trait
406118
Imperium is correct.\n\nEach smell receptor has its own gene.  About 10% of a rat's genome codes for smell receptors, according to howstuffworks.\n\nhttp://science.howstuffworks.com/question139.htm\n\nMost of the similar genes in humans are faulty; we cannot use them.  We get by OK, as our vision is good.  Some experts say that our long history of living with dogs let us benefit from the dog's sense of smell, so we could afford to lose our own.\n\nSee also:\n\nhttp://www.abc.net.au/science/news/stories/s1028434.htm\n\nand\n\nhttp://www.abc.net.au/rn/science/ss/stories/s1330617.htm
1124743
its a genetic problem
667403
Go to this website, you will find all the answers you need:\n\nhttp://plato.stanford.edu/entries/genotype-phenotype/