(Virion is also called) is the virus particle, consists of three parts or two: long molecules carry I), the genetic information in the genetic material made of RNA or DNA; protein layer that protects II), these genes, in some cases lipid envelope that surrounds the coat of ⅲ) extracellular proteins. From the form of the icosahedron and simple helical shape of the virus range of more complex structures. Is about percent of average size average viruses, bacteria. Most viruses, too small to be directly observed with an optical microscope.

In the history of the evolution of life, the origin of the virus is unknown: others may have evolved from the bacteria several possible to be able to move between cells, evolved from the plasmid portion of the DNA There is sex. In evolution, viruses are an important means of horizontal gene transfer to increase the genetic diversity. As they carry genetic material, the virus is considered by some to be reproduced in the form of life will evolve by natural selection. However, (for example, cell structure) is not a main character, which is usually considered, they would be required to count life. As owns a part but not all of these properties, they have been described as “organisms at the end of life” virus.

As aphids is transmitted to plants from plant by insects that it is possible to feed the sap of plants by blood-sucking insects is carried virus in animal virus to spread to be a plant virus is large, in a variety of ways. It is known as the bearing organisms vectors of these diseases. Influenza virus is spread by sneezing and coughing. Feces common cause rotavirus and norovirus, viral gastroenteritis, – It has been sent by the oral route, it enters the body in the water and food, are passed from person to person by contact. HIV is one of the virus or send some by exposure to infected blood through sexual contact. range of host cells capable of viruses infection, called “host range” thereof. Virus If it is possible many kinds are infected widely it, or may be narrowed.

Usually, remove the infecting virus, viral infection in animals to induce an immune response. The immune response can be produced a vaccine for providing adaptive immune artificially certain viral infections. However, some viruses, such as hepatitis and AIDS as a cause of these, you might want to avoid the immune response of these, leading to chronic infection. Antibiotics have no effect on the virus, antiviral drug some have been developed.

Pasteur was not able to guess the pathogen too small to find the cause of rabies, to be detected by using a microscope. 1884, I have invented a filter having microbiologist Charles Chambellan of France, the pores smaller than bacteria. Thus, it is possible to pass a solution containing bacteria through the filter, to remove from the solution entirely. 1892, in order to study what now known as tobacco mosaic virus, biologist Dmitry Ivanovsky in Russia was using this filter. In his experiments, after filtration, the extract from leaves crushed infected tobacco plants indicates that remain infected. There is a possibility toxins produced by the bacteria is due to Ivanovski recommended infection, but does not deal with it. Was thought to be that it can be retained by the filter is an infectious agent, all grown in nutrient medium at the time – this was a part of the germ theory of disease. 1898, solution to repeat the experiment, was filtered, was convinced that a new form of infectious agent is included microbiologist Martinus bay error link in the Netherlands. He multiplied only in cells that have been split the agent, but his efforts did not indicate that it was made of particles, Kontagiumu vivum fluidum it (soluble living germ), he was re-introduced It is pointed out that it is called the word virus. The virus later in nature, they insisted it was a credit theory liquid by a certification Wendell Stanley was particulate Beijerinck. Paul Frosch and Friedrich Loeffler has passed the first animal virus in the same year – agent of foot (Aphthovirus) in the mouth – through a filter similar.

In the early 20th century, to discover a group of viruses that infect bacteria, called (general or phage) bacteriophage, microbiologist Felix d’Herelle French-Canadian, microbiologist Frederick port Wort in the UK that, added to the bacteria now Description agar the virus, it will generate a region of dead bacteria. Dilute suspension of such viruses exactly, (the lowest concentration of virus) was found the highest dilution, but it does not kill all bacteria from different regions of the organism dead it. It counts these regions, multiplying the dilution factor he could calculate the number of viruses in the suspension of the original. Phage, was welcomed as a potential treatment for diseases such as cholera and typhoid fever, but the promise was forgotten in the development of penicillin. The inspection of the phage, and provided insight into the switching a useful mechanism for introducing foreign genes into bacteria and gene.
The end of the 19th century, the virus was determined from the point of view of those infectious filtering, of their requirements for life and a source of power. Virus was grown in plants and animals. 1906, invented a method for growing tissue in lymph, 1928 guinea pig cornea tissue.In, RA Lambert 1913 E. Steinhardt, C., Israel fragments of MC mate and HB-mate Ross Granville Harrison In order to grow the vaccine virus, which was an increase of vaccinia virus in suspension of kidney of minced chicken using this method. The polio virus, their method was not widely adopted until the 1950s when it is grown on a large scale for the production of vaccine. Another breakthrough came in 1931 when a virus or some other influenza grew up in egg chicken pathologist Ernest William Guddopasu of America. 1949, Frederick Robbins John Franklin Enders, and Thomas Weller,, polio virus in cultured cells increased from human embryos, the first virus is grown without the use of eggs and solid animal tissues. This work, was able to make the polio vaccine effective Jonas Salk.

Most of the functionality of the core promoter in eukaryotes have found 25 to 30 base pairs upstream of the TSS is a short DNA sequence known as the box TATA. [QUOTE box TATA is a binding site for transcription factors known protein, a division of transcription factors another called (TFIID) transcription factor II D in sequence (TBP), a TATA binding Promoters basic some. TFIID, after binding to the TATA box by RNA polymerase combine around the TATA box of a series of steps to form a complex before and transcription factors of the two TBP, 5. Because it has two components having a helicase activity, in order to form an initial foam transcription, transcription factor, transcription factor II H is responsible for strand separation of opposing double-stranded DNA. However, the base L, or rate of transcription is driven by the pre-initiation complex alone. Other proteins known as repressor and activator with corepressors or coactivators all related, is responsible for the transfer speed adjusting.

Is substantially homologous to that of eukaryotic transcription to start before the archaea, but is far more complex. Assemble the TATA box binding site in full before initiation complex, but in archaea, the complex, by only (homolog of (TFIIB) transcription factor II B archaea and eukaryotes) TFB RNA polymerase II, and TBP is formed.

Migration feature before starting complex (PIC) to the open complex (yeast ortholog of mammalian XPB) subunit TFIIH SSL2 yeast RNA polymerase II (Pol II) and transcription factor TFIIE general. We form a heterodimer TFA1 (TFIIEα) WH connecting the Tfa2 and Pol II clamp which became one strand complex tandem WH domain bypass promoter DNA is open domain 3 TFIIE wing helix (WH) and (TFIIEβ) I show that. SSL2 is located under cover, to TFIIE near the promoter DNA. In contrast to previous proposals, comparing the model complex and open PIC, very DNA SSL2 suggesting that supplies the 15 base pairs in crevices Pol II, to facilitate the detection of the function as double-stranded DNA translocase are. Strand of DNA by SSL2 channel coupling, to develop an open state and the results of the DNA in combination with downstream of the fixed position of promoter DNA on the right side.

Type II topoisomerase catalyzes the re-connection path and DNA double-strand DNA breaks in order to make the topology change. There is considerable interest in elucidating the role of topoisomerase II, in particular, these proteins, is the target of anti-cancer drugs. Here, to find the role of topoisomerase IIα of RNA polymerase and increased I directed transcription of ribosomal RNA genes to drive the proliferation and cell growth, and in cancer cells. Topoisomerase IIα is a component of the RNA polymerase complex Iβ competent start, our data, interact with the RNA polymerase I-related transcription factor RRN3, which is directed to a polymerase to the promoter in connection SL1 initiation complex formed in advance directly I show that. The B cells, transcriptional activation, is reduced by a reduction in topoisomerase II inhibition or genetic recombination, which is reduced prior to forming the complex with associated double-stranded DNA breaks less transients in the promoter region of rDNA . To generate the rDNA promoter promotion topological modifications effective prior to the de novo transcription initiation complex formation, I topoisomerase IIα offer functionality RNA polymerase.

Assembly, disassembly, and functional properties of transcription before complex from human RNA polymerase I plays an important role in the regulation of rRNA gene expression (image) of (Pol I). For research and process factors employed, spray promoter template assay was developed to allow for isolating the nuclear extracts from the functional image to maintain the exact start of transcription. The pattern immunological factors bound These complexes, suggesting that include initiation of transcription, SL1, factors required for Pol I. (Figure) binding factor upstream In one round of transcription, we have to show that the remaining promoter binding and activists SL1. Furthermore, the promoter, UBF and SL1 were linked to retain the ability to function in initiation of transcription. SL1, has a central role in the stability of the PIC meeting and promoter DNA. Captured image of a template to be recycled efficiently yet be released from the transfer promoter PIC polymerase components immobilized to support transcription of multiple times by promoters “easy” carrying uterine blood flow and SL1 it is possible to resume. Polymerase organized clearance mainly synthesis rate of kinetic analysis of RNA initiation of transcription by Pol revealed that it is limiting the speed step after assembly and recruitment of Pol I. The PIC is Pol I-dependent transcription I It is determined by the rate at which it is listed as starts to escape promoters and transcription. The rate-limiting step of this Pol I transcription, it can be a major target in the regulation of gene expression of rRNA.

The mismatch repair, which contributes to the overall fidelity of DNA replication and to address the impact of damage to the genome is essential. It involves the adjustment of mismatched base pairs have been omitted from the adjustment element of the DNA polymerase. Or practices Azimut protein MutS to modify the loop of small insertion / deletion and point mutations generated in DN A replication time (mutator S), and Mutl the (MMR single) Post-replication mismatch repair system of Escherichia coli with. Mutl of MutS and is involved in preventing recombination between DNA sequences homologous partially. MMR assembly of pieces of MutS, to recognize and bind to, mispaired nucleotide, Azimut and action Mutl will start to by will be able to remove the part of the DNA strand that is synthesized de novo, including the mispaired base further. T mismatch: MutS of a methyl transferase in the repair of O (6) – will be able to cooperate with the damage would be a connection with thymine during replication in order to create a (6) MG if O of methyl guanine other than . Has a conformation monomer there is a difference between the two, to form heterodimers of structure level, MutS is existed as the dimer. Mismatch identifies recognize only one monomer is coupled to ADP. Nonspecific major groove of the DNA binding domain of two monomers include DNA clamp structure. As a consequence of the bracket to move the DNA, uptake and ATP mismatch binding causes a conformational change of the protein MutS.

Has been found in many species, including bacteria (protein and MSH 1,2,3,4,5,6,), and archaea eukaryotes, these proteins, MutS homolog of the family together It is grouped into the MutS. There is considerable diversity of function of MutS family between, but have similar activities of MutS of E. coli Many of these proteins. Encoded species, this diversity is seen in the MutS homolog of the multiple that is equal to a separate many species. Interspecies homologs can be increased through (Mutl a) MutS of horizontal gene transfer of ancient frequently in archaea and eukaryotes from bacteria by symbiotic ancestor of mitochondria and chloroplasts.

This position represents the N-terminal domain of MutS protein family of related proteins closely with DNA mismatch repair protein. N-terminal domain is responsible for MutS mismatch recognition to form chains were mixed six similar structure of the tRNA endonuclease is surrounded by 3α-helix and β sheet. The bacterial protein, yeast MSH3 was predicted protein products of REP-3 gene is involved in DNA mismatch repair, and share sequence similarity of the mouse extensively. MSH in humans is involved in the mismatch-binding protein and (HNPCC) nonpolyposis colon cancer.

Major component mutator phenotype associated with the bacterial strains in some of the defective mismatch repair methyl system is the MutS of Mutl. This system can play an important role in includes both prevention and mismatch repair recombinant homeologous between fragments in E. coli, to adapt to changes in a stressful environment and bacterial population is shown. In this paper, we describe the molecular analysis of gene Mutl and MutS in Staphylococcus aureus. Genetic analysis of mutSL field aureus RN4220 done in S.. Operon structure reversed confirm transcriptase PCR experiments have been reported in gram positive bacteria other.

The inactivation of complementarity and Mutl MutS gene and indicate the role of both genes in hypermutability in this kind of potted plant. In addition, it is designed an in vitro model to study the role of Mutl and MutS in homeologous recombination in Staphylococcus aureus S.. Sensitive PBT1 vector grape soda for this purpose, having a fragment internal temperature cloned in (~ 100% 74%) different levels of identity of the gene S and MutS mutation Mutl and Streptococcus RN4220 is built S. on . You appear to have a limited effect on the control of homeologous recombination Mutl and protein MutS of. Staphylococcus aureus was 11 hypermutable S. analysis, the sequence of the gene and Mutl of MutS, the clinical isolates. In four of the isolates of five with Mutl gene or MutS or deletion mutations, the relationship between the mutator phenotype of change and can be created using the Mutl mutant or MutS’s complement negative.