A mutant is found in which the operon is uninducible. Assuming the affected gene makes a protein, what kind of
824199
activator.\n\ncome on, think about it before you ask for help :P\n\ncould also be a repressor which represses a repressor of the operon in question.  but im sure the answer the asker is looking for is activator.
708384
Go to answers.com and type molecular mutagensis at search you get links go through them.
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.
531423
proto-oncogenes are genes that normally function in regulating proliferation. Mutations that activate them will usually cause the cell to growth without control (this is when we refer to them as oncogenes).\nTumor suppressor genes are caretakers and gatekeepers. They make sure to control uncontrolled proliferation and give the time to a cell to repair any damage. If necessary, wil cause the cell to die. If these genes get mutated then cells would tend to keep unrepaired DNA damages and turn into tumors.
125606
Check this out: \nhttp://www.phschool.com/science/biology_place/biocoach/lacoperon/lactose.html\n\nhttp://www.mun.ca/biochem/courses/4103/topics/lac_operon.html
736240
Your question is unclear.\n\nThe genetic code is the 64 sets of three nucleotides (AGCT) that code for specific amino acids. Due to the codes redundancy, several codons (set of 3 nucleotides) code for the same amino acid, a mutation in the third nucleotide often results in no change in the actual amino acid coded for. These are called "silent mutations" because they have no effect. A mutation in the first or second nucleotide causes a much more dramatic change.
698858
FIrst, using redundant coding, you find the gene by using redundant PCR primers which have the codons coding for the amino acid sequence.  Actually, nowadays, because the human genome is known, you can input the amino acid sequence to the NIH site (and others) and the codon sequence (and gene) which codes for that protein will be determined.  You use specific primers to pull out copies of the gene, and insert them into bacterial vectors- insert coding vectors with the gene into bacteria, and allow the bacteria to produce it in quantity-  Purify it through HPLC, and there you go.
677350
Wow, this answer is gonna be a long one...   There are numerous studies of the charting of the positions of genes on a DNA molecule or chromosome and the distance between genes of Escherisia Coli. It basically comes down to good old conjugation and transduction.  Having sequenced the E. coli K-12 genome, scienctists are creating a knockout of every gene, a clone of every ORF, and an extensive gene expression data set under a variety of physiological conditions. These clones and data sets are made available freely to the community.  Scienctists have also sequenced six additional enterobacterial strains which are pathogens closely related to E. coli K-12, and many plasmids. The comparative genomics aim of this effort is to characterize the gene pool of horizontally transferred elements and virulence determinants known as the pathosphere.\n\nI put a reference on it so be sure to check it out yourself. \n\nA mutator gene, mutD5, whose phenotype is conditional, has been identified in Escherichia coli. By P1 transduction it has been shown to lie at about 5.7 min on the chromosome, being co-transduced with proA and argF. In rich medium, streptomycin- and nalidixic acid-resistant mutation frequencies are 50 to 100 times higher than those in minimal medium. In minimal medium, the mutD5-induced mutation frequencies are still 50 to 100 times above co-isogenic wild-type (mut+) levels. Similar results were obtained with all markers tested. Mutant frequencies can be raised by thymidine in the medium at concentrations as low as 0.04 μM, or by the endogenous generation of thymidine from thymine plus a deoxyribosyl donor. Deoxyadenosine, various ribonucleosides, thymine, and 2-deoxyribose do not stimulate mutation. None of these effects are related to growth rate, since growth rate and mutation rate can be decoupled completely.\n\nThe gntP gene, located between the fim and uxu loci in Escherichia coli K-12, has been cloned and characterized. Nucleotide sequencing of a region encompassing the gntP gene revealed an open reading frame of 447 codons with significant homology to the Bacillus subtilis gluconate permease. Northern (RNA) blotting indicated that the gntP gene was monocistronic and was transcribed as an mRNA with an apparent molecular size of 1.54 kb. The transcriptional start point was determined by primer extension analysis. The gntP gene was found to be under catabolite repression and was not induced by gluconate. Also, expression seemed to be stringently controlled. Several observations indicated that the GntP protein is an inner membrane protein; it contains characteristic membrane-spanning regions and was isolated predominantly from the inner-membrane fraction of fractionated host cells. A topology analysis predicted a protein with 14 membrane-spanning segments. The inability of a mutant strain to grow on gluconate minimal medium could be relieved by introduction of a plasmid encoding the gntP gene. Finally, the kinetics of GntP-mediated gluconate uptake were investigated, indicating an apparent Km for gluconate of 25 microM.
337111
A gene has a Open Reading Frame. An ORF starts with a start codon and ends with a temination codon and it can be grouped into triplet codons and will have a functional protein product.
967608
a. UUACCG (U replaces T in RNA copies) \nb. AAUGGC (the opposite of the above)\nc. A codon is a code for an amino acid. ("3 letters")\nd. The code was copied wrong and therefore a mutation in this case I would say a point mutation because one letter is changed out of the code. This can cause serious problem because it changes the code for an amino acid. It substitution of a single nucleotide. If the code is different but it still codes for the same amino acid it is synonymous and does not causes prob. But if it is the non-synonymous it causes change to the specified amino acid and could lead to production of the WRONG protein or NO protein at all, which is dangerous. These cause genetic disorders such as Sickle cell anemia, cystic fibrosis, tay-sachs.\n\nAdenine bonds with Thymine (in DNA). Adenine with Uracil in RNA. And Guanine and cytosine with each other.\n\nHope this helps :)
659200
I'm not sure what you are asking because of the typos. But here goes an answer for what I think you are trying to ask.\n\nA point mutation involving the addition of a BASE early in the coding, The protein resulting from The gene will be entirely different from the point of addition, since the reading frame will be moved forward. \n\nExample (HYPOTHETICAL)\n\nNormal DNA\nATCGGTACCATT\n\nNormal mRNA\nUAGCCAUGGUAA  The reading frame would be UAG-CCA-UGG-UAA...\n\nmutated mRNA (a C added by mistake)\nUAGCCCAUGGUAA The reading frame would be UAG-CCC-AUG-GUA..\n\nThis can cause the protein to be shorter, because it can create a stop codon somewhere with the addition, also it can make it longer, a stop codon no longer present where it should be.\n\nBasically the protein would be non-functioning.
847901
Mutations can either lead to a loss or gain of function.  Mutations that lead to functional losses are usually recessive, and result in less fit organisms.  Dominant mutations that yield functional gains lead to more fit animals, that produce more viable offspring, which in time, may lead to speciation.
30588
Actually, mutation is normal in every being.\n\nThe genetic code is "divided" (not physically) into TRIPLETS of nitrogened bases. Each triplet codifies for one AMINOACID, which will later form proteins.\n\nNow, the thing is that the same aminoacid can be codified by three or four DIFFERENT triplets. For instance, the aminoacid tryptophan can be codified from the triplets ACU, ACC, ACA and ACG.\n\nAs you may see in that case, the only nitrogen base that changes is the last one (U,C,A,G), but the result of the codification is the same: the aminoacid tryptophan.\n\nSo, in that case, if a mutation occurs in the last nitrogen base, it doesn't really affect anything at all, since tryptophan will still be produced.\n\nThat's what's called a SILENT MUTATION. It has no effect at all in an individual.\n\nThe real problem with mutations start when the first or second nitrogened base of the triplet is mutated. There, the aminoacid that is produced is different that the one is supposed to be produced.\n\nBut even then, if the aminoacid changes the protein (made up from hundreds of aminoacids) might still be the same, without having any effect on the individual.\n\nTo sum up: mutations happen everyday to everyone. The large majority of them has no effect on the general aspect of individuals, and some of them only have minor effects (for example, a mole is the product of a mutation!!!).\n\nWhen they are serious, though, it can lead to any kind of problems, such as cancer and others.\n\nHope it clarified!
943065
it will denature the protein
252508
Organisms do not 'evolve' in response to changes in their environment in order to adapt to that change. Through a process called random mutation, mutant genes are constantly being produced in a small percentage of any given population. If there is no change to the environment, these mutant genes are generally less able to survive than their parent/s. However if there is a sudden or dramatic change, the mutant may be favored over the 'normal' population, because its mutant gene is compatible with the new conditions. This mutant gene now becomes the norm thus ensuring the survival of  its offspring who have inherited this gene.
513720
we're all mutants, that's how things evolve, a mutation in genes
62552
DNA is in every cell, but not every gene is expressed in every cell.  The way that the cell controls which genes are activated and which aren't is through DNA-binding molecules called repressors and promoters.  A promoter binds to DNA near a gene and causes transcription of the gene to make mRNA that will go on to serve as a template for protein synthesis.  Conversely, a repressor can bind to a gene and prevent the transcription of that gene into an RNA template (usually depending on conditions in the cell at the time, like chemical messengers or availability of nutrients, etc.).