DNA repair mechanisms

It is a collection of processes by which DNA repair to identify the cells, to correct the failure of the DNA molecule encoding the genome. In human cells, can cause and normal metabolic activity of both, environmental factors such as radiation and ultraviolet rays can lead to lesions of the molecules of one million individual per day per cell, the DNA damage. Many of these lesions, it is possible to modify the cell’s ability to transfer a gene causing damage to the structure of the DNA molecule encoding a DNA affected, is removed. Other lesion undergoes mitosis and induce mutations potentially harmful to the genome of the cell that affect the survival of its daughter cells. It is always active as a result of the process of DNA repair in response to damage to the DNA structure. When the repair process usually fails, and when the cell apoptosis does not occur, the DNA damage irreparable, may include (ICLS or inter-chain cross-linking), to generate DNA cross-linking and double-strand breaks . Recovery of DNA is dependent on many factors, including the type of cells, the age of the extracellular environment and cells. Or cells, are getting the majority of DNA damage, I can enter one of three states of things, the repaired DNA damage effectively anymore. Also state irreversibly dormancy known as suicide aging cells, known as programmed cell death or apoptosis. Can lead to the formation of tumors in cancer unregulated cell division, DNA repair capacity of the cell, since it is essential for the integrity of the genome, to the body and normal operation. Many genes can affect the life expectancy originally was shown was involved in the protection and repair of DNA damage. It is possible to affect the release rate by the molecular damage uncorrected in the cell forming the gametes to introduce mutations into the genome of the offspring.

Because DNA is a repository of genetic information of living cells of all, the stability and integrity are essential to life. The DNA, however, is not inert, and damage targeting undergraduate attack from the environment, resulting, if it is not repaired, it leads to diseases and possibly mutation. Form of sunlight (in the example perhaps the best known of the connection between the cancer, disease and DNA damage, skin induced by the environment that may be caused by exposure to a lesser extent UV and in, Sun) . Another example is the damage caused by tobacco smoke, which can lead to mutations in lung and subsequent pulmonary cells. May from the agent of the environment, DNA also, to receive metabolism, such as free radicals, by-products apart from oxidative damage. In fact, is that it is possible to make the individual suffer from a change in one million DNA per day.

In addition to gene damage caused by the environment of the process of replication of DNA during cell division, and error-prone. Percentage of the DNA polymerase adds nucleotides erroneous DNA replication at the time is a major factor in determining the spontaneous mutation rate in the body. “Correction” enzyme is generally recognized, while correct many of these errors, several mutations are, survive this process. It estimates the frequency of receiving the correct permanent human DNA errors in the range of 10-6 1 × 10-4 ~ 1 × mutant gametes per gene given. × 10-6 scientist size of 1 is that you will expect to find a mutation in a specific locus of 1 million gametes. Mutations in other organisms have much lower often.

One way can be used to assess the mutation, researchers take into account the speed of the new dominant mutations identified a variety of loci. For example, by examining the population number of individuals had been diagnosed with (disease caused NF1, the non-inherited dominant mutation or spontaneous) neurofibromatosis, researchers spontaneous mutation rate of the gene responsible for this disease is a mutation of 1 × 10-4 average of gametes per found. For example, mutations in other genes, such as that for the treatment of Huntington’s disease, other researchers have found that there was significantly lower than the cost of NF1. The fact that researchers have reported the mutation rate of different genes of another, the locus of some, it appears that failure or other error is more likely to occur.

Many of the proteins present in prokaryotes and eukaryotes, corresponding, DNA repair process is stored in a highly evolved. In fact, such damage, the cells evolved numerous mechanisms to detect and repair various types that might whether due to error or replication environment and impair DNA have. The DNA, since the molecule plays an active role in cell division, the control of DNA repair is associated with cell cycle regulation closely. The DNA cells and cell DNA replication (G1, S, cells. Remembered through the loop consisting of the DNA replication that occurs in mitosis and S phase G2, layer M, in M ​​phase) ensure During mechanism checkpoint cell cycle Before you can split occurs, it is as it is. Damage to these points, you can bring the accumulation of damage leading to mutations in order.

Affect various systems of the body, especially the predisposition of cancer, the number of genetic diseases of humans, defects in DNA repair to the base of the common functions of the constellation. These failures, (AT) ataxia telangiectasia has been included in denatured state engine due to a failure to repair oxidative damage to the cerebellum, xeroderma pigmentosum (XP), or poor sunlight I will repair the damage path state characterized sensitivity to ultraviolet light main relevant (UV). Further, RAD of such groups, the number of genes involved in cancer, the code is also defined an important protein for the repair of DNA damage.

Photoreactivation and NER is not the only way for DNA repair. For example, it is a major mechanism for handling DNA damage spontaneous reactions caused by other species that are generated by free radical metabolism (BER) base excision repair. With offices and operations, you may want to oxidation by reacting with these drugs, resulting in hydrolysis or alkylation. For example, the methyl group (CH 3) chemicals, often 7 – may alternatively be added, purine group be lost to form an methylguanine. All of these changes cause abnormal base that must be removed and replaced. Thus, enzymes known as DNA glycosylase, the bases and sugars that literally – to remove the base-damaged cutting the strand DNA by cleavage of the covalent bond between the phosphate backbone. Then, the polymerase repair fill gap obtained is sealed by ligase. Many of these enzymes are found in cells, each of which is a key specific to certain changes.

Another form of DNA damage is a double-strand breaks, gamma rays, such as X-rays, caused by ionizing radiation. These holidays are very harmful. In addition to preventing the transcription or replication, said portions could lead to chromosomal rearrangements and chromosome, which is attached to other chromosomes. Gene was disrupted in the process leading to inappropriate activation of the gene or fusion protein. Certain types of cancer is associated with such a conversion. Homologous recombination and repair (NHEJ) non-homologous end joining (HRR): double-strand breaks are repaired using either of two mechanisms. In NHEJ, an enzyme called DNA ligase IV using the overhanging portion of the DNA adjacent to the break in order to participate in all fill. If the preparation for the cell is completely isolated, the DNA is not replicated, if there are more errors, it can be introduced during the process. In contrast, the HRR during the homologous chromosomes, and is used as a template for repair.

Mutations in the DNA of the body is part of life. Genetic code we have been exposed to insult the various threatening its integrity. However, strict system of checks and balances, is in place by the DNA repair mechanism. Slip associated with the disease sometimes but errors that They are also a source of changes that are achieved by a long-term process as natural selection and evolution.