Using Biology Workbench if so is it possible to compare two genes? How do you find a mutated version of a gene
817303
Without using molecular methods in a bio lab, you would have to rely on phenotypic testing - ie. the expression of the gene.\n\nin microbiology:\ntest the presence of the gene product and compare them to what is expected\n\nMolecular methods would be more reliable and accurate in detecting a mutation. If you know the sequence of the normal gene you can amplify it by PCR and visualise it by agarose gel elecrophoresis - in which case, the mutated gene would give an altered product if any at all. Or you could use real-time-PCR with a labelled probe complementary to the gene sequence. During the PCR cycle, the probe will bind loosely to the mutated gene but strongly to the natural gene. So during the high temperature stages, the mix with the mutated gene will lose the signal from the probe before the mix with the natural gene.\n\nThere are other methods, but I'm not quite sure what you're dealing with...
995656
Segregate two populations of creatures into separate environments, and see if evolutionary differences between the two populations occur over many generations. That's the sort of experiment the bible thumpers would have to twist logic into a pretzel in order to refute.
713387
REFER TYHIS WEB ADDERESS\nhttp://www.genwaybio.com
348032
When the proteins that copy your DNA make mistakes.  Hence a mutation
882336
Go to your biology book and look it up or go to wikepedia
745603
The expressed gene is the one that shows up.  I have brown hair, but say I have a gene for blonde hair and one for brown.  The expressed gene is brown.
188037
get different genetics
584780
do u want help in ur Bio Data - try monster.com
910758
sorry im a high schooler who doesnt know exactly how to do it but i think to approach it:\n1) find genotype thats just a little bit of guess and check although you know which ones are dominate since they give capital letters and you know they're heterozygous\n2) order youll have to find again with logic and guess and check\n3) genetic distance will be the times that it screws up from what would theoretically happen. Each gene locus in distance is about 1% so the number of percents that accidently cross will be your distance of alleles in map units\n4) this sounds like you would have to do this inorder to get #3... I really dont know too much about this but thats my stab at process of how to solve\nIf there is a pro here, I'd like to know how to do this too
313398
There is no "versus". Mendelian Genetics explained heredity years before when people had funny ideas about inheritance (there was one which said only the father contributed to the children's character and another which said it was the mum!). Biotechnology is using this knowledge as well as knowledge from diverse fields such as Chemistry, Physics, Statistics etc. to modify nature a little for man's benefit. Why the  "versus" question? Both work in tandem.
230567
If the two processes don't copy the templates exactly everytime, that leads to mutations in the following strand.  If there are mutations, that leads to different properties of the proteins made in translation.  Depending on the mutation, this can have either a beneficial or very adverse effect, or even none at all, depending on where the mutation is, and if different amino acids are used.\n\nFor example, sickle cell anemia is caused by a single mutation.  Genotypically, one nucleotide is substituted for another, leading to a different amino acid.  Phenotypically, this different amino acid causes different bonding patterns in the hemoglobin protein, causing red blood cells to sickle.
796672
OK, draw yourself up a nice big checkerboard with 16 squares! Down the left hand side, write beside each square the 4 possible gametes produced by 1 parent - for parents with the genotypes you have given above, the gametes produced are: AB, Ab, aB, ab - this is because each egg or sperm produced will have only half the number of genes of the parent (so ONE copy instead of 2) so that when the egg and sperm meet, they will have 2 copies of each and not more!!! So the gametes will have ONE copy of the 'A' gene (which may be either the dominant 'A' allele or recessive 'a' allele - half the gametes will get one type of allele and half the other) and the same goes for the 'B' gene, to produce the possible gamete types above. Then, along the top of your little checkerboard diagram, write above each of the 4 squares the 4 possible gamete types for the SECOND parent - which in your case, are the same as the first!\n\nNow - you want to fuse your eggs and sperm to produce offspring! Do this by combining the gamete genotype of 1 parent with that of the other in the box where they meet up - eg if your very top left-hand square has the genotype 'AB' above it, and 'AB' to the left of it, then the genotype of the offspring produced will be AABB - homozygous for both! And the square 2 down from the top, in most left column, might be combining the gametes 'Ab' with AB - producing offspring AABb, which is homozygous for gene 'A' but not for gene 'B'.... and so on and so forth for the rest of the squares!\nI WOULD RECOMMEND DRAWING UP THIS SQUARE TO SHOW YOUR WORKING - YOUR TEACHER WILL BE WANTING TO SEE THAT!\ndouble homozygotes are AABB, AAbb, aaBB, or aabb...
512125
in biology, mutations are changes to the genetic material. mutations can be caused by copying errors in the genetic material during cell division and by exposure to radiation, chemicals, or viruses, or can occur deliberately under cellular control during processes such as meiosis or hypermutation. mutations can be classified based on the effect on the structure of the genetic material:\n\n1. small scale mutations affecting one or a few nucleotides\na. point mutation: exchange of a single nucleotide for another through translations or transversions\na)i. silent mutations: code for the same amino acid\na)ii. missense mutations: code for a different amino acid; i.e. sickle cell anemia\na)iii. nonsense mutations: code for a stop codon, which can truncate the protein\nb. insertions: add one or more extra nucleotides causing a shift in the reading frame (or frameshift)\nc. deletions: remove one or more nucleotides thus altering the reading frame (or frameshift)\n\n2. large scale mutations in chromosomal structure\na. amplifications or gene duplications: leading to multiple copies of chromosomal regions\nb. deletions of chromosomal regions: leads to loss of the genes coded; deletions in chromosome 5p causes cri-du-chat syndrome, deletions in chromosome 15q results in prader-willi syndrome\nc. translocations: interchange of genetic parts from non-homologous chromosomes thus bringing together separate genes to form functionally distinct fusion genes; translocations in chromosome 21 causes down syndrome \nd. inversions: reversing the orientation of a chromosomal segment thus bringing together separate genes to form functionally distinct fusion genes\n\nto detect small scale mutations affecting one or more nucleotides, a variety of tests can be done which in principle will test either the dna composition or the presence/absence of the gene products.\n\nlarge scale mutations in the chromosomal structures can be detected using karyotyping because the chromosomes with mutations would differ in sizes and shapes when compared to the standard. in general the chromosomes with deletions would be relatively smaller and chromosomes with additions would be relatively bigger than their counterparts, while chromosomes with either inversions and translocations would exhibit bridges and/or rings.
413968
http://dev.biologists.org/cgi/content/full/130/17/4123?ck=nck
373493
1. Genetic analysis shows similarities among species reflecting evolutionary origins.\n\nThe main point here is that recent work has shown that the extent of genetic divergence among species is consistent with the expected separation based on the fossil record and morphological evidence. This supports the conclusions drawn from the other evidence.\n\nGenetic analysis often reveals remnants of a gene that is functional in one species but not another (i.e. a mutation occurred that made the gene non-functional, but most of the sequence is still intact). Why would God have created non-functional sequences that are extremely similar to functional genes found in related species?\n\nAlso, non-coding regions of DNA show degrees of similarity that are consistent with the expected degree of evolutionary divergence. I understand how you could argue that God was essentially working form a common genetic template for all species, but why change the non-coding regions? These differences result from mutations that do not affect the phenotype of the species in any way but accumulate over time. Non-coding regions show sequences that are conserved with changes, and the number of changes is consistent with the number of mutations that would be expected to have occurred since the approximate time of existence of most recent common ancestor.\n\n2. Many cellular and biochemical processes are conserved in a variety of species.\n\nThe point here is that virtually all cells utilize similar mechanisms of DNA replication and protein synthesis, share certain respiration pathways, and other biochemical processes. Related species show more similarities. For example, all plants are capable of photosynthesis, and utilize a virtually identical biochemical pathway to accomplish this. If you study cell biology you will find numerous examples of pathways that are common to different types of cells. I'm not going to go into this more here as it requires considerable background in cell biology. However, these biochemical similarities support they theory that all cells share a common ancestor.\n\n3. Vestigial biochemical pathways (for example, pancreatic cells are light-sensitive even though they are located deep inside the body).\n\nThese are similar to vestigial structures at the cellular level. The specific example I mentioned is the light-sensitive behavior of pancreatic cells. Basically, the pancreas is located inside the body and will never be exposed to light. However, pancreatic cells grown in vitro (i.e. in a Petri dish, test tube, etc.) demonstrate light-sensitive activation of biochemical pathways similar to that seen in the cells that form the retina. There is no reason for this behavior unless this pathway is a remnant (i.e. a vestigial pathway) of a pathway present in an ancestral cell that did have come in contact with light.\n\nThere are many other examples of vestigial biochemical pathways. Like vestigial structures, their existence is easily explained by evolution but makes no sense in the context of creationism or "intelligent design."
313675
do you mean interactions BETWEEN nucleic acids and proteins?  If so there's a lot of ways you can study that - you can do a footprint analysis - digest the nucleic acid in the presence of the protein and see what piece gets protected to see where the protein binds if you know the identity of the two interacting molecules.  If you don't know their identity you can try a gel-shift assay where DNA will move at different rates on a gel in the presence and absence of various proteins.  If you know the protein but not the DNA you can try an affinity column with the protein immobilized and then try to determine which DNA sequences bind.  You can also try to determine the crystal structure of a co-crystal if you have a lot of the two materials.  good luck!
624134
First, I think a lot of people here don't understand what is meant by the genetic code being the same.  It refers to the ribosomal translation table of codon-->amino acid (for example, AUG-->Met).  I think there actually are some variations, but it's the same in most familiar organisms.\n\nAt the molecular level, proteins evolve a few mutations at a time.  If a gene acquired too many mutations at once, the protein product would almost certainly no longer be functional.  What would happen if you were to change the genetic code in an organism?  You would have widespread mutations in almost every single protein in the organism.  What are the odds that the new organism would be capable of surviving?  Very, very low.\n\nThe basic principle is that genes that are absolutely critical for life evolve the slowest.  Thus, the genetic code has not changed as much as other things.