why is thymine necessary for DNA repair?
462830
Expecting you to know the structure of DNA...\nthe enigmatic enzyme known as DinB DNA polymerase is specialized for proficient and accurate replication of a particular kind of damaged DNA.\nDNA is assaulted daily by toxic chemicals, metabolic byproducts, sunlight, and other forms of radiation. Most of the nicks and dings are quickly fixed by the cell's fleet of precision DNA repair processes, which can surgically excise and replace a faulty section. \nBut sometimes a damaged bit of DNA slips through unrepaired. A faulty nucleotide—the basic constituent of DNA—can stall the temperamental DNA replication machinery as it unwinds and copies the genome in dividing cells. In humans, uncorrected DNA errors passed along to the new daughter cells can lead to cancer. \n\nWhen DNA integrity is at stake, a family of proteins known as translesion DNA polymerases comes to the rescue. They cannot actually repair a damaged strand of DNA, but they can smooth over the problem by inserting a nucleotide opposite the damaged partner, so the DNA replication machinery can finish duplicating the chromosome despite the damaged DNA. This trick is usually referred to as a DNA damage tolerance mechanism.\nThe molecular building blocks of DNA are adenine, cytosine, guanine, thymine - A, C, G, and T in the shorthand of molecular biology. In different combinations, they make up the genes that code for the proteins that carry out the routine and complex tasks necessary for life.\nthe enzyme DinB is exceptionally skilled at copying over a particular kind of damage to the G nucleotide. When the main DNA replication machinery stalls at the damaged G, the DinB translesion polymerase recognizes the G and adds its chemical partner, C, to form the correct base pair in the new chromosome.\na single change in the amino acids that make up DinB will strip it of its unique talent and change it into an ordinary polymerase.
906596
Post Replication Repair Mechanism - DNA Repair\n\nThe reconstruction of a continuous two-stranded DNA molecule without mismatch from a molecule which contained damaged regions.  The major repair mechanisms are excision repair, in which defective regions in one strand are excised and resynthesized using the complementary base pairing information in the intact strands; photo reactivation repair, in which the lethal and mutagen effects of ultraviolet light are eliminated; and post -replication repair, in which the primary lesions are not repaired, but the gaps in one daughter duplex are filled in by incorporation of portions of the other (undamaged) daughter duplex.  Excision repair and post-replication repair are sometimes referred to as "dark repair" because they do not require light.
353863
Like any other mutation.  DNA damage usually, or chromosomal problems such as nondisjunction.  Often p53 will be inactivated by multiple different mechanisms including deletion of the chromosomal region (chr17 in humans I believe), and point mutations of the coding region of the gene.  DNA damage is promoted by loss of repair pathways (due to mutation, etc), but is caused by UV radiation, or IR radiation, or other stress such as chemotherapy drugs, or carcinogens.  DNA damage can occur numerous ways, and there are many different repair pathways.  The damage has to first occur, then be 'missed' by repair pathways, and then the damage has to be at a critical region (ie p53), to promote tumorogenesis.
845407
RNA polymerase is necessary for making RNA from DNA and is found in pretty much all organs, cells, and viruses.\n\ndoes this help?
283053
Each cell contains our DNA makeup, it is protected inside the cell from bacteria, viruses and other harmful agents.  Without DNA our body would not be able to replicate and replace the cells which make up for example our organs or skin.  We are constantly producing new skin cells to replace the ones that we shed off every second.
374804
Consider a regular climbing ladder.  If the ladder was sawed in half by sawing each rung crosscut thru the middle than each half of the ladder would represent one  DNA strand.  Each new organism receives a single strand from each of it's parents.  The two strands join to make the new organism's double stranded DNA.  The rail or sides of the ladder would represent the sugar and phosphate link backbone of the DNA.  The sawed rung would represent the nucleic acid bases.  The bases are classified as either purines or pyrimidines.  The two purines are Adenine (A) and Guanine (G) which are similiar to the compound Purine.  The two pyrimidine bases are Thymine (T) and Cytosine (C) which are structured similiar to the compound Pyrimidine.  In RNA Thymidine is replaced by Uracil.  The collective term for these structures is "nitrogenous base".  Each base contains either/or hydrogen (h), nitrogen (n) and oxygen (o) atoms located on the structure where the "cut" would exhist on the sawed ladder rungs.  When these bases move close together there is an attraction between these atoms and a bridge forms called a hydrogen bond  or h-bond.Thymine has an o and a h.  Adenine has a h which is attracted to T's o and an n which is attracted to T' h. A and T always h-bond or pair.  Cytosine has an h,n,and o.  Guanine has two h's and an o.  one h on guanine is attracted to the o on cytosine, the other to the n.  The o is attracted to the h on cytosine.  Therefore C always pairs with G and is held together by three h-bonds, where A and T are paired by two h-bonds.  In total the h-bonds strongly bind the two DNA single strands together but one at a time they can be broken to seperate the strands much like a zipper opening link by link.  Since C always pairs with G their proportion is is always the same.  The same is true for A and T.  Each Dna single strand has what is called a 3' (three prime hydroxyl) and a 5' (five prime phosphate) end.  When the two single strands pair to form thd Double strand they Form with the 3' end of one strand joining at the 5' end of the other strand.  This is known as antiparallel since they are running in opposite directions.
794419
Alkylating agents add alkyl groups to electronegative groups, cross-linking guanine nucleotides in DNA.\n\nExamples: Busulfan, cyclophosphamide, carmustine.
871261
Exposure to sun is important for people because it triggers the production of vitamin D, necesary in the absotion and balance of calcium (which is basic for life). Black people in poorly lit places (say finland...) have calcium problems. \nThe amount of energy necesary for this, however is not big. The problem with sunlight is that it has a lot of UV radiation that can produce mutations in the DNA. if the exposure is too strong, the amount of mutation will be so big that the cell will simply die (this is when you peel at the beach, layers of skin cells died and falled down). this mutations in the skin cells DNA can produce many deseases, beeing cancer the most conspicous one. \nMelanin, the skin pigment, is a very good absorber of UV radiation, so black people don't have problems in high radiation places, whereas whities need to be extremely carefull.
299525
DNA viruses often require the host cells' machinery in order to replicate their genomes.  Most cells in your body have stopped dividing and no longer make the proteins required to replicate DNA.  Therefore, the viruses have evolved mechanisms to reactivate the genes encoding for these proteins.  Unfortunately, this can also lead to reactivation of DNA replication of the host cell, uncontrolled cell division, and ultimately cancer.  RNA viruses, on the other hand, need to make their own proteins to replicate their genomes since the host cells often do not possess the machinery to replicate RNA.  Therefore, RNA viruses do not need to activate pathways in the host cell that may cause cancer.
61314
There are several possible answers. I don't think you really needed the words "somatoplasm" and "germplasm" in your question. Those are sort of obscure terms, and technically they refer to the cytoplasm in either a somatic cell or a germ cell, when I think you really meant to refer to the cells themselves. A somatic cell is any cell in the body that is not a reproductive cell, and a germ cell, or a gamete, is a sperm or egg or a precursor (which I can tell you know, but I thought I'd make things less obscure).\n\nSo in a way, your question contains its own answer. A germline mutation would be a change in the DNA in a cell that is going to become an egg or sperm. This sort of mutation is one that could be passed on to the offspring, assuming that the mutation was not lethal. It would be observed in the next generation if it was dominant, and not masked by supressor genes.\n\nA somatic mutation could have several outcomes. There are several systems of DNA repair machinery that would first try to repair the damage. If these failed, certain types of damage would trigger a process known as apoptosis, which is basically a self destruct sequence for the cell. This keeps damaged cells from causing additional damage. When mutations affect either the DNA repair pathways, the apoptosis pathway, or both, they can lead to cancer by allowing defective cells to survive.\n\nThe outcome of a somatic mutation is going to depend on what is mutated though. In an adult, where pretty much all of your cells have decided what they are going to be and have become that type of cell (neuron, muscle, skin, etc), certain genetic programs will be on or off in each cell. If there is a mutation in something the cell doesn't need, it might not notice. Then again, if the mutation causes something to be turned on when it should be off, that could cause problems, and again, that is exactly the sort of thing that leads to cancer.\n\nThere are a lot of interesting asides to this question, so if you are curious about other aspects of mutations, ask away...
93891
The important thing is to keep the helical structure clearly visible. Don't worry about the side hydrogens or details of the molecules.\n\nKeep in mind that DNA is a double-stranded helix, and the strands don't revolve around each other identically. Which means there are two sizes of 'grooves': the small grooves are a bit over half the width of the large ones.\n\nIf you use styrofoam balls for the nucleotides and join them with drinking straws (a handy way to do this project), take care that the angle subtended by three of the balls be around 35 degrees.\n\nAbout 10 balls should complete a cycle, which means ball number 11 must be above ball number 1 in a straight line.\n\nDo a strand first, so that it looks fairly twisted yet linear. Add the other strand afterwards. A length of about 20 nucleotides per strand (= 40 in total = 40 small styrofoam balls) should be enough.\n\nGo to a crafts store and buy a bag of balls (they come in 50, 100, etc.) and a bag of 100 drinking straws. Color the balls blue for cytosine, red for thymine, green for guanine and orange for adenine. Pair orange with red and blue with green when building the second strand.\n\nHope this helps.
52398
All bases are present in DNA except URACIL and in RNA it is THYMINE. Adenine is joined with Thymine in DNA, as well as Cytosine is with Guanine. In RNA, The only difference is that Adenine Joins with Uracil. Guanine and Cytosine still Join together.
825920
No other information need be given.\n\nThe diagram represents a "untwisted" double helix.  The top row is a series of nitrogen bases, and the bottom row would be it's complimentary half.  The question is asking you which nitrogen base is paired with or across the ladder from Guanine in DNA. \n\nGuanine is a purine, and purines only bond with pyrimidines.  Since Adenine is also a purine, that is the incorrect answer.  Cytosine, thymine and uracil are pyrimidines.  Uracil is only found in RNA, so since the question specifies DNA, Uracil is incorrect.  That leaves us cytosine and thymine.  \n\nThe correct answer is (C) cytosine.  Guanine and cytosine are held together through three hydrogen bonds.  Adenine and thymine (or uracil in RNA) are joined by only two hydrogen bonds.  The molecules do not line up properly between guanine and thymine to form a bond.
765843
There is a very cool way to demonstrate the S phase of the cell cycle.  There is a chemical compound BrdU (Bromodioxy uridine) that can act as a replacement for genetic thymadine.  If you inject the animal undergoing S phase with Brdu, it will be incorporated into the replicated DNA.  You can then label that chemical with either Immunofluorescence or Immunohistochemical reagents that will either make the label visible because it fluoresces under specific light conditions or will stain a dark color and be visible in a light microscope.
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To combat free radicals\n-----------------\nIn biological systems, the normal processes of oxidation (plus a minor contribution from ionizing radiation) produce highly reactive free radicals. These can readily react with and damage other molecules. In some cases the body uses free radicals to destroy foreign or unwanted objects, such as in an infection. However, in the wrong place, the body's own cells may become damaged. Should the damage occur to DNA, the result could be cancer. Antioxidants decrease the damage done to cells by reducing oxidants before they can damage the cell.\n\nVirtually all studies of mammals have concluded that a restricted calorie diet extends the lifespan of mammals by as much as 100%. This remarkable finding suggests that food is actually more damaging than smoking. As food produces free radicals (oxidants) when metabolized, antioxidant-rich diets are thought to stave off the effects of aging significantly better than diets lacking in antioxidants. The reduced levels of free radicals, resulting from a reduction in their production by metabolism, is thought to be a major cause of the success of caloric restriction in increasing life span.\n\nFree radical damage in the mitochondria of living cells is a byproduct of oxidative phosphorylation. Superoxide radicals are generated, which can damage mitochodrial and mitochondrial membranes. Unlike DNA in the cell nucleus, mitochondrial DNA has only a few DNA-repair enzymes and the DNA is not protected by histones.\n\nMany antioxidants, however (including vitamin C and vitamin E) can't get into mitochondria for various reasons (e.g. because they are too hydrophilic to cross mitochondrial membranes or too hydrophobic to cross the cytoplasm). Melatonin is an important natural antioxidant that has been demonstrated [citation needed] to strongly protect mitochondria from damage. A group of scientists in Russia (led by V. Skulachev) have created a custom antioxidant (a Skulachev ion forms the point of the molecule and penetrates the mitochondrial membrane; the antioxidising part is attached behind it) that can enter the mitochondria and stays there due to the membrane potential gradient; preventing damage to DNA.\n\nAlthough there is little doubt that antioxidants are a necessary component for good health, there is considerable doubt as to the most beneficial antioxidant(s) and as to the optimal amount for results. A study of lung cancer patients found that those given antioxidant supplements had worse prognoses. This is believed to be due to antioxidant interference with the body's normal use of localised free radicals e.g. Nitric oxide for cell signalling. Due to the complex nature of the interactions of antioxidants with the body, it is difficult to interpret the results of many experiments designed to test such things. In vitro testing (outside the body) has shown many natural antioxidants, in specific concentration, can halt the growth of or even kill cancerous cells.\n\nFor example, recent studies are suggesting that at high levels, synthetic antioxidant vitamins such as A, E and C may prove to have pro-oxidant effects: increasing the formation of free radicals. The fact that natural antioxidants are always ingested together with a wide variety of flavonoids and other phytochemicals also likely plays a part. Many supplement manufacturers supply more expensive tablets containing these. Newer liquid nutritional supplements using plant ionic compounds are believed to be more readily absorbed in the human body.\n\nThe benefits of antioxidants were examined during the Age-Related Eye Disease Study.\n\nNutritional antioxidants\nThe following substances have shown positive antioxidant effects:\n\nVitamin A (Retinol, also synthesized by the body from beta-carotene) protects dark green, yellow and orange vegetables and fruits from solar radiation damage, and is thought to play a similar role in the human body. Carrots, squash, broccoli, sweet potatoes, tom
1128100
they are both important in erythrocytes production..if lack of those,the DNA malproduced in the process of making erythrocytes.Thus causing anemia..\n\nThe body cannot absorb these when the person had done stomach bypass,resection of the stomach among others..
143311
Mutation not nutation\nIn biology, mutations are changes to the genetic material (usually DNA or RNA). 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 the processes such as meiosis or hypermutation. In multicellular organisms, mutations can be subdivided into germline mutations, which can be passed on to progeny and somatic mutations, which cannot be transmitted to progeny. Mutations, when accidental, often lead to the malfunction or death of a cell and can cause cancer. Mutations are considered the driving force of evolution, where less favorable (or deleterious) mutations are removed from the gene pool by natural selection, while more favorable (beneficial or advantageous) ones tend to accumulate. Neutral mutations are defined as mutations whose effects do not influence the fitness of either the species or the individuals who make up the species. These can accumulate over time. Contrary to tales of science fiction, the overwhelming majority of mutations have no significant effect, since DNA repair is able to revert most changes before they become permanent mutations, and many organisms have mechanisms for eliminating otherwise permanently mutated somatic cells.\n\nBy effect on structure\nThe DNA sequence of a gene can be altered in a number of ways. Gene mutations have varying effects on health, depending on where they occur and whether they alter the function of essential proteins. Structurally, mutations can be classified as:\n\nSmall-scale mutations affecting one or a few nucleotides, including: \nPoint mutations, often caused by chemicals or malfunction of DNA replication, exchange a single nucleotide for another. Most common is the transition that exchanges a purine for a purine (A ↔ G) or a pyrimidine for a pyrimidine, (C ↔ T). A transition can be caused by nitrous acid, base mispairing, or mutagenic base analogs such as 5-bromo-2-deoxyuridine (BrdU). Less common is a transversion, which exchanges a purine for a pyrimidine or a pyrimidine for a purine (C/T ↔ A/G). A point mutation can be reversed by another point mutation, in which the nucleotide is changed back to its original state (true reversion) or by second-site reversion (a complementary mutation elsewhere that results in regained gene functionality). These changes are classified as transitions or transversions. An example of a transversion is adenine being converted into a cytosine. There are also many other examples that can be found. Point mutations that occur within the protein coding region of a gene may be classified into three kinds, depending upon what the erroneous codon codes for: \nsilent mutations: codes for the same amino acid \nmissense mutations: codes for a different amino acid \nnonsense mutations: codes for a stop, which can truncate the protein \nInsertions add one or more extra nucleotides into the DNA. They are usually caused by transposable elements, or errors during replication of repeating elements (e.g. AT repeats). Insertions in the coding region a gene may alter splicing of the mRNA, or cause a shift in the reading frame (frameshift), both of which can significantly alter the gene product. Insertions can be reverted by excision of the transposable element. \nDeletions remove one or more nucleotides from the DNA. Like insertions, these mutations can alter the reading frame of the gene. They are irreversible. \nLarge-scale mutations in chromosomal structure, including: \nAmplifications (or gene duplications) leading to multiple copies of chromosomal regions, increasing the dosage of the genes located within them. \nDeletions of large chromosomal regions, leading to loss of the genes within those regions. \nMutations whose effect is to juxtapose previously separate pieces of DNA, potentially bringing together separate genes to form functionally distinct fusion genes (e.g. bcr-abl). These