query: where does the process of replication occur in the cell

pos: DNA replication phage T4 DNA elongation in phage-infected "E. coli". During the period of exponential DNA increase at 37 °C, the rate was 749 nucleotides per second. The mutation rate per base pair per replication during phage T4 DNA synthesis is 1.7 per 10. DNA replication, like all biological polymerization processes, proceeds in three enzymatically catalyzed and coordinated steps: initiation, elongation and termination. For a cell to divide, it must first replicate its DNA. This process is initiated at particular points in the DNA, known as "origins", which are targeted by initiator proteins. In "E. coli" this protein is DnaA; in yeast,

pos: Bruce William Stillman made up of six subunits that binds to cellular origins of DNA replication and coordinates the entire process of initiating a complete cycle of DNA replication throughout the entire cell genome. Soon after the discovery of ORC, Stillman’s group identified other initiation proteins that together form the pre-replication complex (pre-RC), which makes chromosomes competent for the subsequent initiation of DNA replication during the S phase of the cell cycle. His group’s recent studies have revealed the intricate details of the mechanism of the initiation of DNA replication and illuminated how this process is regulated throughout the cell cycle, including the

pos: Licensing factor Licensing factor A licensing factor is a protein or complex of proteins that allows an origin of replication to begin DNA replication at that site. They are thought to primarily occur in eukaryotic cells, since prokaryotes use simpler systems to initiate replication. Origins of replication represent start sites for DNA replication and so their "firing" must be regulated to maintain the correct karyotype of the cell in question. The origins are required to fire only once per cell cycle, an observation that led to the postulated existence of licensing factors by biologists in the first place. If the origins were

pos: DNA replication independently of the cell cycle, through the process of D-loop replication. In vertebrate cells, replication sites concentrate into positions called replication foci. Replication sites can be detected by immunostaining daughter strands and replication enzymes and monitoring GFP-tagged replication factors. By these methods it is found that replication foci of varying size and positions appear in S phase of cell division and their number per nucleus is far smaller than the number of genomic replication forks. P. Heun et al.(2001) tracked GFP-tagged replication foci in budding yeast cells and revealed that replication origins move constantly in G1 and S phase and

pos: Replication timing called DNA replication origins, followed by an unzipping process that unwinds the DNA as it is being copied. However, replication does not start at all the different origins at once. Rather, there is a defined temporal order in which these origins fire. Frequently a few adjacent origins open up to duplicate a segment of a chromosome, followed some time later by another group of origins opening up in an adjacent segment. Replication does not necessarily start at exactly the same origin sites every time, but the segments appear to replicate in the same temporal sequence regardless of exactly where within

pos: Replisome remains at a fixed, midcell location in the cell, attached to the membrane, and the template DNA threads through it. DNA is fed through the stationary pair of replisomes located at the cell membrane. For eukaryotes, numerous replication bubbles form at origins of replication throughout the chromosome. As with prokaryotes, two replisomes are required, one at each replication fork located at the terminus of the replication bubble. Because of significant differences in chromosome size, and the associated complexities of highly condensed chromosomes, various aspects of the DNA replication process in eukaryotes, including the terminal phases, are less well-characterised than for

neg: Cell (biology) the S phase of the cell cycle. In meiosis, the DNA is replicated only once, while the cell divides twice. DNA replication only occurs before meiosis I. DNA replication does not occur when the cells divide the second time, in meiosis II. Replication, like all cellular activities, requires specialized proteins for carrying out the job. Between successive cell divisions, cells grow through the functioning of cellular metabolism. Cell metabolism is the process by which individual cells process nutrient molecules. Metabolism has two distinct divisions: catabolism, in which the cell breaks down complex molecules to produce energy and reducing power, and

neg: Orthoreovirus change. After uncoating is completed, the active virus is released in the cytoplasm where replication of the genome and virion takes place. Replication of the virus takes places in the cytoplasm of the host cell. Since the genome of this virus is dsRNA, early transcription of the genome must take place inside the capsid where it is safe and will not be degraded by the host cell. dsRNA inside of a cell is a tip off to the immune system that the cell is infected with a virus, since dsRNA does not occur in the normal replication of a cell.

neg: Centrosome cycle. During the prophase in the process of cell division called mitosis, the centrosomes migrate to opposite poles of the cell. The mitotic spindle then forms between the two centrosomes. Upon division, each daughter cell receives one centrosome. Aberrant numbers of centrosomes in a cell have been associated with cancer. Doubling of a centrosome is similar to DNA replication in two respects: the semiconservative nature of the process and the action of CDK2 as a regulator of the process. But the processes are essentially different in that centrosome doubling does not occur by template reading and assembly. The mother centriole

neg: DNA re-replication and Cdc6 expression. Loss of p53 regulation in cells can also be observed frequently in cell lines that overexpress Cdt1 or Cdc6. For the special case of cell cycle-regulated DNA replication in which DNA synthesis is uncoupled from cell cycle progression refer to endoreduplication. Endoreduplication is an important and widespread mechanism in many cell types. It does not adhere to many of the cell cycle checkpoints and damage controls in regularly dividing cells, but it does not result in uncontrolled re-replication. Endoreduplication is a controlled process and occurs to perform a specific cell function. In some cells, it has been

neg: Viral replication Viral replication Viral replication is the formation of biological viruses during the infection process in the target host cells. Viruses must first get into the cell before viral replication can occur. Through the generation of abundant copies of its genome and packaging these copies, the virus continues infecting new hosts. Replication between viruses is greatly varied and depends on the type of genes involved in them. Most DNA viruses assemble in the nucleus while most RNA viruses develop solely in cytoplasm. Viruses multiply only in living cells. The host cell must provide the energy and synthetic machinery and the low

neg: Cell division chromosomes must be replicated, and the duplicated genome must be separated cleanly between cells. A great deal of cellular infrastructure is involved in keeping genomic information consistent between generations. Interphase is the process a cell must go through before mitosis, meiosis, and cytokinesis. Interphase consists of three main stages: G1, S, and G2. G1 is a time of growth for the cell where specialized cellular functions occur in order to prepare the cell for DNA Replication. There are checkpoints during interphase that allow the cell to be either progressed or denied further development. In S phase, the chromosomes are replicated

neg: Gene germ cells, ensuring variation in the next generation. Although Mendelian inheritance remains a good model for many traits determined by single genes (including a number of well-known genetic disorders) it does not include the physical processes of DNA replication and cell division. The growth, development, and reproduction of organisms relies on cell division; the process by which a single cell divides into two usually identical daughter cells. This requires first making a duplicate copy of every gene in the genome in a process called DNA replication. The copies are made by specialized enzymes known as DNA polymerases, which "read" one

neg: Viral replication with the help of the host cell's polymerases This small group of viruses, exemplified by the Hepatitis B virus, have a double-stranded, gapped genome that is subsequently filled in to form a covalently closed circle (cccDNA) that serves as a template for production of viral mRNAs and a subgenomic RNA. The pregenome RNA serves as template for the viral reverse transcriptase and for production of the DNA genome. Viral replication Viral replication is the formation of biological viruses during the infection process in the target host cells. Viruses must first get into the cell before viral replication can occur. Through

neg: Monoclonal by the progeny. Common usages of this term include: Monoclonal Monoclonal cells are a group of cells produced from a single ancestral cell by repeated cellular replication. Thus they can be said to form a single clone. The term "monoclonal" comes from the Ancient Greek "monos", meaning "alone" or "single", and "klon", meaning "twig". The process of replication can occur "in vivo", or may be stimulated "in vitro" for laboratory manipulations. The use of the term typically implies that there is some method to distinguish between the cells of the original population from which the single ancestral cell is derived,

neg: Monoclonal Monoclonal Monoclonal cells are a group of cells produced from a single ancestral cell by repeated cellular replication. Thus they can be said to form a single clone. The term "monoclonal" comes from the Ancient Greek "monos", meaning "alone" or "single", and "klon", meaning "twig". The process of replication can occur "in vivo", or may be stimulated "in vitro" for laboratory manipulations. The use of the term typically implies that there is some method to distinguish between the cells of the original population from which the single ancestral cell is derived, such as a random genetic alteration, which is inherited

neg: CHEK1 cellular responses to HIV infection and somatic cell viability. Chk1 is essential for the maintenance of genomic integrity. Chk1 monitors DNA replication in unperturbed cell cycles and responds to genotoxic stress if present. Chk1 recognizes DNA strand instability during replication and can stall DNA replication in order to allow time for DNA repair mechanisms to restore the genome. Recently, Chk1 has shown to mediate DNA repair mechanisms and does so by activating various repair factors. Furthermore, Chk1 has been associated with three particular aspects of the S-phase, which includes the regulation of late origin firing, controlling the elongation process and

neg: Cell growth briefly at M phase when the nucleus and then the cell divide in two. The process of cell division, called cell cycle, has four major parts called phases. The first part, called G phase is marked by synthesis of various enzymes that are required for DNA replication. The second part of the cell cycle is the S phase, where DNA replication produces two identical sets of chromosomes. The third part is the G phase in which a significant protein synthesis occurs, mainly involving the production of microtubules that are required during the process of division, called mitosis. The fourth phase,

neg: Psoralen ICLs introduced by psoralen are highly genotoxic to actively replicating cells. The covalent linkage impedes replication fork progression. Thus unlinking the ICL is required before replication can resume. The initial steps in repair ordinarily involve incisions in one parental strand on both sides of the crosslink. Subsequently, repair of the lesion can occur by an accurate or an inaccurate process. The accurate process for repairing crosslinks is homologous recombinational repair (HRR). This involves replacing the damaged information using the intact information from another homologous chromosome in the same cell. "Escherichia coli" cells deficient in HRR are highly sensitive to PUVA

neg: Pre-replication complex Pre-replication complex A pre-replication complex (pre-RC) is a protein complex that forms at the origin of replication during the initiation step of DNA replication. Formation of the pre-RC is required for DNA replication to occur. Complete and faithful replication of the genome ensures that each daughter cell will carry the same genetic information as the parent cell. Accordingly, formation of the pre-RC is a very important part of the cell cycle. As organisms evolved and became increasingly more complex, so did their pre-RCs. The following is a summary of the components of the pre-RC amongst the different domains of life.

neg: Replication timing with relative ease indicates that we will soon have a wealth of information about where and when large changes in chromosome folding occur during development and in different diseases. Replication timing Replication timing refers to the order in which segments of DNA along the length of a chromosome are duplicated. In eukaryotic cells (cells that package their DNA within a nucleus), chromosomes consist of very long linear double-stranded DNA molecules. During the S-phase of each cell cycle (Figure 1), all of the DNA in a cell is duplicated in order to provide one copy to each of the daughter cells

neg: Epstein–Barr virus cell. Unlike B-cell entry, epithelial-cell entry is actually impeded by viral glycoprotein gp42. Once EBV enters the cell, the viral capsid dissolves and the viral genome is transported to the cell nucleus. The lytic cycle, or productive infection, results in the production of infectious virions. EBV can undergo lytic replication in both B cells and epithelial cells. In B cells, lytic replication normally only takes place after reactivation from latency. In epithelial cells, lytic replication often directly follows viral entry. For lytic replication to occur, the viral genome must be linear. The latent EBV genome is circular, so it must

neg: Replication timing each segment replication starts. Figure 2 shows a cartoon of how this is generally envisioned to occur, while Figure 3 shows an animation of when different segments replicate in one type of human cell. The temporal order of replication of all the segments in the genome, called its replication-timing program, can now be easily measured in two different ways. One way simply measures the amount of the different DNA sequences along the length of the chromosome per cell. Sequences that duplicate first, long before cell division, will be more abundant in each cell than the sequences that replicate last just

neg: Host tropism This process further produces memory B cell and memory T cells that allow long-lasting immunity to occur. In conclusion, if a pathogen is capable of overcoming various host defenses, recognizing a host cell for infection, and successfully replicating within a host tissue, then the pathogen is likely to possess tropism for that specific host. Viral host tropism is determined by a combination of susceptibility and permissiveness: a host cell must be both permissive (allow viral replication) and susceptible (possess the receptor complement needed for viral entry) for a virus to establish infection. Once a virus binds to a host cell,

neg: S phase rapidly degraded. This immediately halts histone production and prevents a toxic buildup of free histones. Free histones produced by the cell during S-phase are rapidly incorporated into new nucleosomes. This process is closely tied to the replication fork, occurring immediately in “front” and “behind” the replication complex. Translocation of MCM helicase along the leading strand disrupts parental nucleosome octamers, resulting in the release of H3-H4 and H2A-H2B subunits. Reassembly of nucleosomes behind the replication fork is mediated by chromatin assembly factors (CAFs) that are loosely associated with replication proteins. Though not fully understood, the reassembly does not appear to utilize

neg: Schizosaccharomyces pombe Wee1, preventing phosphorylation of Cdk1 and thereby leading to activation of CDK and mitotic entry. (This simplified diagram omits several other regulators of CDK activity.) Fission yeast switches mating type by a replication-coupled recombination event, which takes place during S phase of the cell cycle. Fission yeast uses intrinsic asymmetry of the DNA replication process to switch the mating type; it was the first system where the direction of replication was shown to be required for the change of the cell type. Studies of the mating-type switching system lead to a discovery and characterization of a site-specific replication termination site

neg: Pre-replication complex to cause Meier-Gorlin syndrome, which is characterized by absent or hypoplastic patellae, small ears, impaired pre- and post-natal growth, and microcephaly. Known mutations are in the ORC1, ORC4, ORC6, CDT1, and CDC6 genes. The disease phenotype probably originates from reduced ability of cells to proliferate, reduced cell number, and general growth failure. Pre-replication complex A pre-replication complex (pre-RC) is a protein complex that forms at the origin of replication during the initiation step of DNA replication. Formation of the pre-RC is required for DNA replication to occur. Complete and faithful replication of the genome ensures that each daughter cell will

neg: Mamavirus Mamavirus possesses its own transcription machinery, and it packages transcription proteins in its particles. Transcription is believed to occur in the core particles. The core releases viral DNA and forms a cytoplasmic replication factory where DNA replication begins and transcription of late genes occurs. The replication factory forms around the viral core and expands until it occupies a large fraction of the amoeba cell volume. Later stages of the replication cycle involve partially assembled procapsids undergoing DNA packaging. While the mimiviridae were a surprise themselves, mamavirus contained an even bigger surprise. While looking at mamavirus under the electron microscope, Raoult

neg: Oncovirus the Hepatitis B virus (an RNA virus) inactivates p53 by sequestering it in the cytoplasm. SV40 has been well studied and does not cause cancer in humans, but a recently discovered analogue called Merkel cell polyomavirus has been associated with Merkel cell carcinoma, a form of skin cancer. The Rb binding feature is believed to be the same between the two viruses. In the 1960s, the replication process of RNA virus was believed to be similar to other single-stranded RNA. Single-stranded RNA replication involves RNA-dependent RNA synthesis which meant that virus-coding enzymes would make partial double-stranded RNA. This belief was

neg: Extrachromosomal DNA ribosomal DNA and telomere DNA. Certain organisms, such as yeast, rely on chromosomal DNA replication to produce eccDNA whereas eccDNA formation can occur in other organisms, such as mammals, independently of the replication process. The function of eccDNA has not been widely studied, but it has been proposed that the production of eccDNA elements from genomic DNA sequences adds to the plasticity of the eukaryotic genome and can influence genome stability, cell aging and the evolution of chromosomes. Viral DNA is an example of extrachromosomal DNA. Understanding viral genomes is very important for understanding the evolution and mutation of the

neg: Cancer of a gene and affect its expression, or may occur in the gene's coding sequence and alter the function or stability of its protein product. Disruption of a single gene may also result from integration of genomic material from a DNA virus or retrovirus, leading to the expression of "viral" oncogenes in the affected cell and its descendants. Replication of the data contained within the DNA of living cells will probabilistically result in some errors (mutations). Complex error correction and prevention is built into the process and safeguards the cell against cancer. If a significant error occurs, the damaged cell

neg: Eukaryotic DNA replication divided into the daughter cells at mitosis. The major enzymatic functions carried out at the replication fork are well conserved from prokaryotes to eukaryotes, but the replication machinery in eukaryotic DNA replication is a much larger complex, coordinating many proteins at the site of replication, forming the replisome. The replisome is responsible for copying the entirety of genomic DNA in each proliferative cell. This process allows for the high-fidelity passage of hereditary/genetic information from parental cell to daughter cell and is thus essential to all organisms. Much of the cell cycle is built around ensuring that DNA replication occurs without

neg: Coenocyte mycelia in which hyphae lack septa are known as "aseptate" or "coenocytic". Many insects, such as the model organism "Drosophila melanogaster", lay eggs that initially develop as "syncytial" blastoderms, i.e. early on the embryos exhibit incomplete cell division. The nuclei undergo S-phase (DNA replication) and sister chromatids get pulled apart and re-assembled into nuclei containing full sets of homologous chromosomes, but cytokinesis does not occur. Thus, the nuclei multiply in a common cytoplasmic space. The early embryo "syncytium" of invertebrates such as "Drosophila" is important for "syncytial" specification of cell differentiation. The egg cell cytoplasm contains localized mRNA molecules such

neg: Idaeovirus end. The first ORF encodes for a cell-to-cell movement protein, while the second ORF is expressed as a subgenomic RNA strand. This strand, RNA-3, is 946 nucleotides in length and encodes for the coat protein. Infection has been shown to not occur if RNA-3 is either not present or is sufficiently damaged. Viral replication is cytoplasmic. Entry into the host cell is achieved by penetration into the host cell. Replication follows the positive stranded RNA virus replication model. Positive stranded RNA virus transcription is the method of transcription. The virus exits the host cell by tubule-guided viral movement. Plants serve

neg: Cell damage structural alterations, mutations ordinarily involve the normal four bases in new arrangements. Mutations can be replicated, and thus inherited when the DNA replicates. In contrast, DNA damages are altered structures that cannot, themselves, be replicated. Several different repair processes can remove DNA damages (see chart in DNA repair). However, those DNA damages that remain un-repaired can have detrimental consequences. DNA damages may block replication or gene transcription. These blockages can lead to cell death. In multicellular organisms, cell death in response to DNA damage may occur by a programmed process, apoptosis. Alternatively, when a DNA polymerase replicates a template strand

neg: Antineoplastic resistance response to imatinib mesylate. Determining areas of gene amplification in cells from cancer patients has huge clinical implications. Gene deletion is the opposite of gene amplification, where a region of a chromosome is lost an drug resistance occurs by losing tumor suppressor genes such as "TP53." Genomic instability can occur when the replication fork is disturbed or stalled in its migration. This can occur with replication fork barriers, proteins such as PTIP, CHD4 and PARP1, which are normally cleared by the cell´s DNA damage sensors, surveyors, and responders BRCA1 and BRCA2. Epigenetic modifications in antineoplastic drug resistance play a major

neg: Large tumor antigen the nucleus where it performs its replication-related functions. The OBD binds the viral genome's origin of replication by recognizing specific sequences that occur in the portion of the viral genome known as the non-coding control region. It also forms interactions with host cell proteins, such as replication protein A and Nbs1. The OBD is required for viral replication. The zinc-binding and ATPase domains together comprise the helicase portion of the LTag protein. The primary function of the zinc-binding domain is oligomerization of LTag. Formation of dodecamer structures (two hexameric rings) is required for helicase activity, which begins at the origin

neg: Central dogma of molecular biology faithful, deterministic transfers, wherein one biopolymer's sequence is used as a template for the construction of another biopolymer with a sequence that is entirely dependent on the original biopolymer's sequence. In the sense that DNA replication must occur if genetic material is to be provided for the progeny of any cell, whether somatic or reproductive, the copying from DNA to DNA arguably is the fundamental step in the central dogma. A complex group of proteins called the replisome performs the replication of the information from the parent strand to the complementary daughter strand. The replisome comprises: This process typically takes

neg: Microevolution are caused by radiation, viruses, transposons and mutagenic chemicals, as well as errors that occur during meiosis or DNA replication. Errors are introduced particularly often in the process of DNA replication, in the polymerization of the second strand. These errors can also be induced by the organism itself, by cellular processes such as hypermutation. During the process of DNA replication, errors occasionally occur in the polymerization of the second strand. These errors, called mutations, can affect the phenotype of an organism, especially if they occur within the protein coding sequence of a gene. Error rates are usually very low—1 error

neg: Cell growth features of the three types of cell reproduction that either involve binary fission, mitosis, or meiosis. The diagram below depicts the similarities and differences of these three types of cell reproduction. The DNA content of a cell is duplicated at the start of the cell reproduction process. Prior to DNA replication, the DNA content of a cell can be represented as the amount Z (the cell has Z chromosomes). After the DNA replication process, the amount of DNA in the cell is 2Z (multiplication: 2 x Z = 2Z). During Binary fission and mitosis the duplicated DNA content of the

neg: Mitosis interphase nuclei. During mitotic progression, typically after the anaphase onset, the cell may undergo cytokinesis. In animal cells, a cell membrane pinches inward between the two developing nuclei to produce two new cells. In plant cells, a cell plate forms between the two nuclei. Cytokinesis does not always occur; coenocytic (a type of multinucleate condition) cells undergo mitosis without cytokinesis. The mitotic phase is a relatively short period of the cell cycle. It alternates with the much longer "interphase", where the cell prepares itself for the process of cell division. Interphase is divided into three phases: G (first gap), S

neg: Viral replication molecular-weight precursors for the synthesis of viral proteins and nucleic acids. The virus replication occurs in seven stages, namely; The virus attaches to the cell membrane of the host cell. It then injects its DNA or RNA into the host to initiate infection. In animal cells these viruses get into the cell through the process of endocytosis which works through fusing of the virus and fusing of the viral envelope with the cell membrane of the animal cell and in plant cell it enters through the process of pinocytosis which works on pinching of the viruses. The cell membrane of

neg: DNA replication DNA replication In molecular biology, DNA replication is the biological process of producing two identical replicas of DNA from one original DNA molecule. This process occurs in all living organisms and is the basis for biological inheritance. The cell possesses the distinctive property of division, which makes replication of DNA essential. DNA is made up of a double helix of two complementary strands. During replication, these strands are separated. Each strand of the original DNA molecule then serves as a template for the production of its counterpart, a process referred to as semiconservative replication. As a result of semi-conservative replication,

neg: Human bocavirus rolling hairpin mechanism that is dependent on the NS1 protein. Replication results in the creation of a series of circular head to tail sequences. A sequence conserved among the Parvoviridae TAAAAAT is found close to the 3' terminus. Other parvoviruses replicate only when the host cell is in S phase: viral replication results in the death of the host cell. This pattern has not yet been experimentally confirmed for the bocaviruses but seems likely to be the case. Expression of the viral proteins alone does not cause host cell death. unlike other parvoviruses where this has been examined. The receptor

neg: Caulobacter crescentus the chromosome. The CtrA protein, in contrast, acts to block initiation of replication, so it must be removed from the cell before chromosome replication can begin. Multiple additional regulatory pathways integral to cell cycle regulation and involving both phospho signaling pathways and regulated control of protein proteolysis act to assure that DnaA and CtrA are present in the cell just exactly when needed. Each process activated by the proteins of the cell cycle engine involve a cascade of many reactions. The longest subsystem cascade is DNA replication. In "Caulobacter" cells, replication of the chromosome involves about 2 million DNA synthesis

neg: Pangenesis was thought to occur by some sort of a 'mutual affinity.' Each gemmule was said to be specifically related to a certain body part- as described, they did not contain information about the entire organism. The different types were assumed to be dispersed through the whole body, and capable of self-replication given ‘proper nutriment'. When passed on to offspring via the reproductive process, gemmules were thought to be responsible for developing into each part of an organism and expressing characteristics inherited from both parents. Darwin thought this to occur in a literal sense: he explained cell proliferation to progress as

neg: Mesosome also hypothesized to aid in photosynthesis, cell division, DNA replication, and cell compartmentalisation. These models were called into question during the late 1970s when data accumulated suggesting that mesosomes are artifacts formed through damage to the membrane during the process of chemical fixation, and do not occur in cells that have not been chemically fixed. By the mid to late 1980s, with advances in cryofixation and freeze substitution methods for electron microscopy, it was generally concluded that mesosomes do not exist in living cells. However, a few researchers continue to argue that the evidence remains inconclusive, and that mesosomes might

neg: Azacitidine through the carbon-5 atom, but this latter reaction does not occur with azacytosine because its carbon-5 is substituted by nitrogen, leaving the enzyme covalently bound to DNA and blocking its DNA methyltransferase function. In addition, the covalent protein adduction also compromises the functionality of DNA and triggers DNA damage signaling, resulting in the degradation of trapped DNA methyltransferases. As a consequence, methylation marks become lost during DNA replication. Azacitidine causes anemia (low red blood cell counts), neutropenia (low white blood cell counts), and thrombocytopenia (low platelet counts), and patients should have frequent monitoring of their complete blood counts, at least

neg: Pre-replication complex to bind the AT-rich portion of the origin of replication in "S. pombe" using AT hook motifs. The mechanism of origin recognition in higher eukaryotes is not well understood but it is thought that the ORC1-6 proteins depend on unusual DNA topology for binding. Assembly of the pre-replication complex only occurs during late M phase and early G1 phase of the cell cycle when cyclin-dependent kinase (CDK) activity is low. This timing and other regulatory mechanisms ensure that DNA replication will only occur once per cell cycle. Assembly of the pre-RC relies on prior origin recognition, either by DnaA in

neg: Germline mutation somatic or germline cells, but not both. A germline mutation often arises due to endogenous factors, like errors in cellular replication and oxidative damage. This damage is rarely repaired imperfectly, but due to the high rate of germ cell division, can occur frequently. Endogenous mutations are more prominent in sperm than in ova. This is because spermatocytes go through a larger number of cell divisions throughout a male’s life, resulting in more replication cycles that could result in a DNA mutation. Errors in maternal ovum also occur, but at a lower rate than in paternal sperm. The types of mutations

neg: Lichen planus when concomitant oral or genital lesions occur, significantly affects patients’ quality of life. The cause of lichen planus is unknown, but it is not contagious and does not involve any known pathogen. It is thought to be a T cell mediated autoimmune reaction (where the body's immune system targets its own tissues). This autoimmune process triggers apoptosis of the epithelial cells. Several cytokines are involved in lichen planus, including tumor necrosis factor alpha, interferon gamma, interleukin-1 alpha, interleukin 6, and interleukin 8. This autoimmune, T cell mediated, process is thought to be in response to some antigenic change in the

neg: Eukaryotic DNA replication up to 2 to 3 nucleotides of DNA or RNA ahead of its polymerization, generating a short "flap" substrate for Fen1, which can remove nucleotides from the flap, one nucleotide at a time. By repeating cycles of this process, DNA polymerase δ and Fen1 can coordinate the removal of RNA primers and leave a DNA nick at the lagging strand. It has been proposed that this iterative process is preferable to the cell because it is tightly regulated and does not generate large flaps that need to be excised. In the event of deregulated Fen1/DNA polymerase δ activity, the cell

neg: DNA replication site-binding protein, or Ter protein. Because bacteria have circular chromosomes, termination of replication occurs when the two replication forks meet each other on the opposite end of the parental chromosome. "E. coli" regulates this process through the use of termination sequences that, when bound by the Tus protein, enable only one direction of replication fork to pass through. As a result, the replication forks are constrained to always meet within the termination region of the chromosome. Within eukaryotes, DNA replication is controlled within the context of the cell cycle. As the cell grows and divides, it progresses through stages in

neg: Helper dependent virus safe for use in gene therapy since an infection cannot occur except in the presence of a suitable helper virus. Well established protocols allow scientists to propagate helper dependent viruses in the lab. However, using an actual helper virus poses problems when it comes to purification of a desired transgenic virus. Therefore, lab methods often utilize minimal fragments of the helper DNA that can serve this purpose without creating unwanted virus. This process usually involves the introduction of three separate DNA plasmids into a eukaryotic cell line through a process called transfection. These plasmids contain either transgenic DNA or replication

neg: Hayflick limit proliferating; Hayflick called this the time of "luxuriant growth". After months of doubling the cells eventually reach phase three, a phenomenon he named "senescence", where cell replication rate slows before halting altogether. The Hayflick limit has been found to correlate with the length of the telomeric region at the end of chromosomes. During the process of DNA replication of a chromosome, small segments of DNA within each telomere are unable to be copied and are lost. This occurs due to the uneven nature of DNA replication, where leading and lagging strands are not replicated symmetrically. The telomeric region of DNA

neg: Replication timing Replication timing Replication timing refers to the order in which segments of DNA along the length of a chromosome are duplicated. In eukaryotic cells (cells that package their DNA within a nucleus), chromosomes consist of very long linear double-stranded DNA molecules. During the S-phase of each cell cycle (Figure 1), all of the DNA in a cell is duplicated in order to provide one copy to each of the daughter cells after the next cell division. The process of duplicating DNA is called DNA replication, and it takes place by first unwinding the duplex DNA molecule, starting at many locations

neg: DNA replication the cell cycle; DNA replication takes place during the S phase (synthesis phase). The progress of the eukaryotic cell through the cycle is controlled by cell cycle checkpoints. Progression through checkpoints is controlled through complex interactions between various proteins, including cyclins and cyclin-dependent kinases. Unlike bacteria, eukaryotic DNA replicates in the confines of the nucleus. The G1/S checkpoint (or restriction checkpoint) regulates whether eukaryotic cells enter the process of DNA replication and subsequent division. Cells that do not proceed through this checkpoint remain in the G0 stage and do not replicate their DNA. Replication of chloroplast and mitochondrial genomes occurs

neg: Spindle checkpoint divide, because cell size is big enough or because they receive the appropriate stimulus, they activate the mechanism to enter into the cell cycle, and they duplicate most organelles during S (synthesis) phase, including their centrosome. Therefore, when the cell division process will end, each daughter cell will receive a complete set of organelles. At the same time, during S phase all cells must duplicate their DNA very precisely, a process termed DNA replication. Once DNA replication has finished, in eukaryotes the DNA molecule is compacted and condensed, to form the mitotic chromosomes, each one constituted by two sister chromatids,

neg: Mammalian orthoreovirus resulting in the exposure of micro1, a membrane-penetration mediator, as well as a conformational change in the σ1 attachment protein. After the uncoated virus particles penetrate the endosomes, early transcription of the double stranded RNA genome by viral polymerase occurs inside the uncoated (naked) viral core. This process occurs in this manner so the viral double stranded RNA is not exposed to the cytoplasm, as this would cause the cell to attack the viral particle. The viral core is then released into the cytoplasm of the host cell, where replication occurs. Replication is completed with the aid of protein λ3,

neg: Small tumor antigen and LTag interact through their J domains with Hsc70 to increase its ATPase activity. Because polyomavirus genome replication relies on the DNA replication machinery of the host cell, the cell must be in S phase (the part of the cell cycle in which the host cell's genome is normally replicated) in order to provide the necessary molecular machinery for viral DNA replication. Viral proteins therefore promote dysregulation of the cell cycle and entry into S phase. This function is usually primarily provided by LTag through its interactions with retinoblastoma protein and p53. STag contributes to this process through its interaction

neg: T7 phage too short to span the cell envelope and, in order to eject the phage genome into the cell at the initiation of infection, virion proteins must first make a channel from the tip of the tail into the cell cytoplasm. The phage also injects proteins needed to begin replication of the viral genome and cleave the host genome. T7 bacteriophage overcomes several of the host bacteria's defenses including the peptidoglycan cell wall and the CRISPR system. Once the T7 phage has inserted the viral genome the process of DNA replication of the host genome is halted and replication of viral

neg: Raccoonpox virus From here it must enter into the cytoplasm. The replication of RCN occurs in the cytoplasm- never in the nucleus. Replication and Transcription: The replication and transcription of the viral genome occur in the cytoplasm. Genome replication begins with the uncoating of the virus core as it comes into contact with the plasma membrane. Once uncoated, the viral DNA is expressed and replication follows. Replication of the RCN genome occurs through the strand displacement method. Assembly and Release: Viral assembly occurs in the cytoplasm. The release of the mature virus particle always results in lysing of the host cell. RCN

neg: Bacteria made during the replication of DNA or from exposure to mutagens. Mutation rates vary widely among different species of bacteria and even among different clones of a single species of bacteria. Genetic changes in bacterial genomes come from either random mutation during replication or "stress-directed mutation", where genes involved in a particular growth-limiting process have an increased mutation rate. Some bacteria also transfer genetic material between cells. This can occur in three main ways. First, bacteria can take up exogenous DNA from their environment, in a process called transformation. Many bacteria can naturally take up DNA from the environment, while

neg: Eukaryotic DNA replication to the fact that CDK levels remain high during the S phase, G, and M phases of the cell cycle no new pre-RC complexes can be formed. This all helps to ensure that no initiation can occur until the cell division is complete. In addition to cyclin dependent kinases a new round of replication is thought to be prevented through the downregulation of Cdt1. This is achieved via degradation of Cdt1 as well as through the inhibitory actions of a protein known as geminin. Geminin binds tightly to Cdt1 and is thought to be the major inhibitor of re-replication. Geminin

neg: Eukaryotic DNA replication completes copying the region. There are programmed replication fork barriers (RFBs) bound by RFB proteins in various locations, throughout the genome, which are able to terminate or pause replication forks, stopping progression of the replisome. DNA replication is a tightly orchestrated process that is controlled within the context of the cell cycle. Progress through the cell cycle and in turn DNA replication is tightly regulated by the formation and activation of pre-replicative complexs (pre-RCs) which is achieved through the activation and inactivation of cyclin-dependent kinases (Cdks, CDKs). Specifically it is the interactions of cyclins and cyclin dependent kinases that are

neg: Eukaryotic DNA replication expressed. Transition into the S-phase indicates replication has begun. In order to preserve genetic information during cell division, DNA replication must be completed with high fidelity. In order to achieve this task, eukaryotic cells have proteins in place during certain points in the replication process that are able to detect any errors during DNA replication and are able to preserve genomic integrity. These checkpoint proteins are able to stop the cell cycle from entering mitosis in order to allow time for DNA repair. Checkpoint proteins are also involved in some DNA repair pathways, while they stabilize the structure of the

neg: Thogotovirus additional amino acids at its C-terminus. No product has yet been identified for the seventh segment, observed in DHOV. The receptor on the vertebrate host cell is sialic acid, which is bound by the viral glycoprotein. Entry is by endocytosis, with fusion of the viral and cell membranes occurring once the vesicle is acidified. In common with other orthomyxoviruses, viral transcription and replication both occur in the cell nucleus. In some members of the genus, replication has been shown to be sensitive to the Mx1/MxA protein, which is induced in mice and humans in response to interferon. In one study,

neg: Umatilla virus the dsRNA never comes in direct contact with the cytoplasm, early replication occurs in the viral core. Both replication and assembly occur in the cytoplasm of the host cell. Host ribosomes are used to translate the viral RNA into mRNA. Virions self-assemble in they host cell cytoplasm and then exit by budding following host cell death. This virus is transmitted by ticks, mosquitoes, or sand flies and has a range of hosts with the most common being cattle and birds. Umatilla virus Umatilla virus (UMAV) is a dsRNA virus in the family "Reoviridae", subfamily "Sedoreovirinae", and the genus "Orbivirus". This

neg: Cyanophages from photosynthetic metabolism of the host cell. Lysing of the host cell tends to occur after the completion of host DNA replication and immediately prior to cell division. This is due to the increased availability of resources for the replication of viral particles. Certain cyanophages infect and burst "Prochlorococcus", the world's smallest and most abundant primary producers. Marine cyanophages of the family "Myoviridae" help regulate primary production mainly through infection of "Synechococcus" spp. The other two families, "Podoviridae" and "Siphoviridae", are usually found in freshwater ecosystems. In coastal oceans, abundance of viruses infecting "Synechococcus" spp. can reach >10 mL and

neg: Polyomaviridae the viral capsid structure is likely to be disrupted by action of host cell disulfide isomerase enzymes. The details of transit to the nucleus are not clear and may vary among individual polyomaviruses. It has been frequently reported that an intact, albeit distorted, virion particle is released from the endoplasmic reticulum into the cell cytoplasm, where the genome is released from the capsid, possibly due to the low calcium concentration in the cytoplasm. Both expression of viral genes and replication of the viral genome occur in the nucleus using host cell machinery. The early genes - comprising at minimum the

neg: Adenoviridae "in vitro" allowing E1B (binds p53 tumor suppressor) to assist and stably transform the cells. Nevertheless, they are reliant upon each other to successfully transform the host cell and form tumors. DNA replication separates the early and late phases. Once the early genes have liberated adequate virus proteins, replication machinery, and replication substrates, replication of the adenovirus genome can occur. A terminal protein that is covalently bound to the 5’ end of the adenovirus genome acts as a primer for replication. The viral DNA polymerase then uses a strand displacement mechanism, as opposed to the conventional Okazaki fragments used in

neg: DNA base flipping repair mechanisms, and DNA replication. It can also occur in RNA double helices or in the DNA:RNA intermediates formed during RNA transcription. DNA base flipping occurs by breaking the hydrogen bonds between the bases and unstacking the base from its neighbors. This could occur through an active process, where an enzyme binds to the DNA and then facilitates rotation of the base, or a passive process, where the base rotates out spontaneously, and this state is recognized and bound by an enzyme. It can be detected using X-ray crystallography, NMR spectroscopy, fluorescence spectroscopy, or hybridization probes. Base flipping was first

neg: Polyomaviridae small tumor antigen (ST) and large tumor antigen (LT) - are expressed first, from a single alternatively spliced messenger RNA strand. These proteins serve to manipulate the host's cell cycle - dysregulating the transition from G1 phase to S phase, when the host cell's genome is replicated - because host cell DNA replication machinery is needed for viral genome replication. The precise mechanism of this dysregulation depends on the virus; for example, SV40 LT can directly bind host cell p53, but murine polyomavirus LT does not. LT induces DNA replication from the viral genome's non-coding control region (NCCR), after which

neg: Eukaryotic DNA replication by the association of histone H2A-H2B. This process is thought to occur through the FACT complex, since it already associated with the replisome and is able to bind free H2A-H2B, or there is the possibility of another H2A-H2B chaperone, Nap1. Electron microscopy studies show that this occurs very quickly, as nucleosomes can be observed forming just a few hundred base pairs after the replication fork. Therefore, the entire process of forming new nucleosomes takes place just after replication due to the coupling of histone chaperones to the replisome. When compared to prokaryotic DNA replication, the completion of eukaryotic DNA replication

neg: Cell division cycle 7-related protein kinase done at this point to try to fix the CDC7 gene so replication can occur. By copying and replacing the altered area with a very similar area on the sister homolog chromosome, the gene can be replicated as if nothing was ever wrong on the chromosome. However, when the cell enters this arrested state, levels of p53 may increase. These increased levels of p53 may initiate cell death. After chromatin undergoes changes in telophase of mitosis, the hexameric protein complex of MCM proteins 2-7 forms part of the pre-replication complex (pre-RC) by binding to the chromatin and other aiding proteins

neg: Cyclin A makes chromatin capable of replication. When the amount of cyclin A/CDK2 complex reaches a threshold level, it terminates the assembly of the pre-replication complex made by cyclin E/CDK2. As the amount of Cyclin A/CDK2 complex increases, the complex initiates DNA replication. Cyclin A has a second function in S phase. In addition to initiating DNA synthesis, Cyclin A ensures that DNA is replicated once per cell cycle by preventing the assembly of additional replication complexes. This is thought to occur through the phosphorylation of particular DNA replication machinery components, such as CDC6, by the cyclin A/CDK2 complex. Since the action

neg: Chlamydia (genus) also take the form of a reticulate body, which is in fact an intracytoplasmic form, highly involved in the process of replication and growth of these bacteria. The reticulate body is slightly larger than the elementary body and may reach up to 0.6 μm in diameter with a minimum of 0.5 μm. It does not present a cell wall. When stained with iodine, reticulate bodies appear as inclusions in the cell. The DNA genome, proteins, and ribosomes are retained in the reticulate body. This occurs as a result of the development cycle of the bacteria. The reticular body is basically

neg: Self-replication Self-replication Self-replication is any behavior of a dynamical system that yields construction of an identical copy of itself. Biological cells, given suitable environments, reproduce by cell division. During cell division, DNA is replicated and can be transmitted to offspring during reproduction. Biological viruses can replicate, but only by commandeering the reproductive machinery of cells through a process of infection. Harmful prion proteins can replicate by converting normal proteins into rogue forms. Computer viruses reproduce using the hardware and software already present on computers. Self-replication in robotics has been an area of research and a subject of interest in science fiction.

neg: Caulobacter crescentus pathways is to ensure reliable production and elimination of the CtrA protein from the cell at just the right times in the cell cycle. An essential feature of the "Caulobacter" cell cycle is that the chromosome is replicated once and only once per cell cycle. This is in contrast to the "E. coli" cell cycle where there can be overlapping rounds of chromosome replication simultaneously underway. The opposing roles of the "Caulobacter" DnaA and CtrA proteins are essential to the tight control of "Caulobacter" chromosome replication. The DnaA protein acts at the origin of replication to initiate the replication of

neg: Cell division in the first division, and sister chromatids are separated in the second division. Both of these cell division cycles are used in the process of sexual reproduction at some point in their life cycle. Both are believed to be present in the last eukaryotic common ancestor. Prokaryotes (bacteria) undergo a vegetative cell division known as binary fission, where their genetic material is segregated equally into two daughter cells. All cell divisions, regardless of organism, are preceded by a single round of DNA replication. For simple unicellular microorganisms such as the amoeba, one cell division is equivalent to reproduction – an

neg: Okazaki fragments prokaryotic E. coli chromosome has only a single origin of replication. Replication in prokaryotes occurs inside of the cytoplasm, and this all begins the replication that is formed of about 100 to 200 or more nucleotides. Eukaryotic DNA molecules have a significantly larger number of replicons, about 50,000 or more; however, replication does not occur at the same time on all of the replicons. In eukaryotes, DNA replication takes place in the nucleus. A plethora replication form in just one replicating DNA molecule, the start of DNA replication is moved away by the multi-subunit protein. This replication is slow, and

neg: Nuclear DNA prophase, metaphase, anaphase, and telophase. A key difference, however, is that during meiosis, each of these phases occurs twice — once during the first round of division, called meiosis I, and again during the second round of division, called meiosis II. Prior to cell division, the DNA material in the original cell must be duplicated so that after cell division, each new cell contains the full amount of DNA material. The process of DNA duplication is usually called replication. The replication is termed semiconservative since each new cell contains one strand of original DNA and one newly synthesized strand of

neg: Viroplasm infection. For example, viroplasms of mimivirus have a similar size to the nucleus of its host, the amoeba "Acanthamoeba polyphaga". A virus can induce changes in composition and organization of host cell cytoskeletal and membrane compartments, depending on the step of the viral replication cycle. This process involves a number of complex interactions and signaling events between viral and host cell factors. Viroplasms are formed early during the infection; in many cases, the cellular rearrangements caused during virus infection lead to the construction of sophisticated inclusions —viroplasms— in the cell where the factory will be assembled. The viroplasm is where

neg: SeqA protein domain SeqA protein domain In molecular biology the protein domain SeqA is one found in bacteria and archaea. The function of this protein domain is highly important in DNA replication. The protein negatively regulates the initiation of DNA replication at the origin of replication, in "Escherichia coli", OriC. Additionally the protein plays a further role in sequestration. The importance of this protein is vital, without its help in DNA replication, cell division and other crucial processes could not occur. This protein domain is thought to be part of a much larger protein complex which includes other proteins such as SeqB. DNA

neg: DNA repair daughter cells after it undergoes mitosis. As a consequence, the DNA repair process is constantly active as it responds to damage in the DNA structure. When normal repair processes fail, and when cellular apoptosis does not occur, irreparable DNA damage may occur, including double-strand breaks and DNA crosslinkages (interstrand crosslinks or ICLs). This can eventually lead to malignant tumors, or cancer as per the two hit hypothesis. The rate of DNA repair is dependent on many factors, including the cell type, the age of the cell, and the extracellular environment. A cell that has accumulated a large amount of DNA

neg: Reoviridae several proteins which are needed for replication and conversion of the dsRNA genome into (+)-RNAs. The virus can enter the host cell via a receptor on the cell surface. The receptor is not known but is thought to include sialic acid and junctional adhesion molecules (JAMs). The virus is partially uncoated by proteases in the endolysosome, where the capsid is partially digested to allow further cell entry. The core particle then enters the cytoplasm by a yet unknown process where the genome is transcribed conservatively causing an excess of (+) sense strands, which are used as mRNA templates to synthesize

neg: Viral protein replication process itself. Similarly, during the assembly of viruses, some of these proteins also carry out important functions that affect the assembly process. Some of these viral nonstructural protein functions are replicon formation, immunomodulation, and transactivation of viral structural protein encoding genes. Viral nonstructural proteins interact with host cell proteins to form the replicon, otherwise known as the replication complex. In the hepatitis C virus, viral nonstructural proteins interact with cellular vesicle membrane transport protein, hVAP-33, to assemble the replicon. Viral nonstructural 4b (NS4B) protein alters the host cell's membrane and starts the formation process of the replication complex. Other

neg: Frameshift mutation mechanisms present in a cell to ensure the correct transfer of genetic information during the process of DNA replication as well as during translation, mutations do occur; frameshift mutation is not the only type. There are at least two other types of recognized point mutations, specifically missense mutation and nonsense mutation. A frameshift mutation can drastically change the coding capacity (genetic information) of the message. Small insertions or deletions (those less than 20 base pairs) make up 24% of mutations that manifest in currently recognized genetic disease. Frameshift mutations are found to be more common in repeat regions of DNA.

neg: Tetrahymena fixed for a particular trait, in a process called phenotypic assortment. In this way, the polyploid genome can fine-tune its adaptation to environmental conditions through gain of beneficial mutations on any given mini-chromosome whose replication is then selected for, or conversely, loss of a minichromosome which accrues a negative mutation. However, the macronucleus is only propagated from one cell to the next during the asexual, vegetative stage of the life cycle, and so it is never directly inherited by sexual progeny. Only beneficial mutations that occur in the germline micronucleus of "T. thermophila" are passed down between generations, but these

neg: Eukaryotic DNA replication starts elongation, initiation starts in second replicon. Now, if the first replicon moves in clockwise direction, the second replicon moves in anticlockwise direction, until "T" of first replicon is reached. At "T", both the replicons merge to complete the process of replication. Meanwhile, the seco nond replicon is moving in forward direction also, to meet with the third replicon. This clockwise and counter-clockwise movement of two replicons is termed as bidirectional replication. Eukaryotic DNA replication requires precise coordination of all DNA polymerases and associated proteins to replicate the entire genome each time a cell divides. This process is achieved through

neg: DNA repair regular helical structure by introducing non-native chemical bonds or bulky adducts that do not fit in the standard double helix. Unlike proteins and RNA, DNA usually lacks tertiary structure and therefore damage or disturbance does not occur at that level. DNA is, however, supercoiled and wound around "packaging" proteins called histones (in eukaryotes), and both superstructures are vulnerable to the effects of DNA damage. DNA damage can be subdivided into two main types: The replication of damaged DNA before cell division can lead to the incorporation of wrong bases opposite damaged ones. Daughter cells that inherit these wrong bases carry

neg: DNA adduct a piece of DNA that has DMBA attached to it. The presence of such an adduct indicates prior exposure to a potential carcinogen, but does not by itself indicate the presence of cancer in the subject animal. Chemicals that form DNA adducts include: DNA adducts include: By-products include: When a chemical binds to DNA, the DNA becomes damaged, and proper and complete replication cannot occur to make the normal intended cell. This could be the start of a mutation, or mutagenesis. Without effective DNA repair, which happens naturally under normal circumstances, this can lead to carcinogenesis, the beginnings of cancer.

neg: Bacterial conjugation enzyme is called TraI and the relaxosome consists of TraI, TraY, TraM and the integrated host factor IHF. The nicked strand, or "T-strand", is then unwound from the unbroken strand and transferred to the recipient cell in a 5'-terminus to 3'-terminus direction. The remaining strand is replicated either independent of conjugative action (vegetative replication beginning at the "oriV") or in concert with conjugation (conjugative replication similar to the rolling circle replication of lambda phage). Conjugative replication may require a second nick before successful transfer can occur. A recent report claims to have inhibited conjugation with chemicals that mimic an intermediate

neg: Viral transformation of the host cell's replication machinery; therefore, many viral genes have promoters that support binding of many transcription factors found naturally in the host cells. These transcription factors along with the virus' own proteins can repress or activate genes from both the virus and the host cell's genome. Many viruses can also increase the production of the cell's regulatory proteins. Depending on the virus, a variety of genetic changes can occur in the host cell. In the case of a lytic cycle virus, the cell will only survive long enough to the replication machinery to be used to create additional

neg: Eukaryotic DNA replication of their localization to the replication fork. Loading of Mcm proteins can only occur during the G of the cell cycle, and the loaded complex is then activated during S phase by recruitment of the Cdc45 protein and the GINS complex to form the active Cdc45–Mcm–GINS (CMG) helicase at DNA replication forks. Mcm activity is required throughout the S phase for DNA replication. A variety of regulatory factors assemble around the CMG helicase to produce the ‘Replisome Progression Complex’ which associates with DNA polymerases to form the eukaryotic replisome, the structure of which is still quite poorly defined in comparison

neg: Lucy Shapiro cell, has a tail-like flagellum that helps it swim; the other daughter has a stalk which anchors it to a surface. Swarmer cells become stalked cells after a short period of motility. Chromosome replication and cell division only occur in stalked cells. Rather than containing an evenly dispersed mixture of proteins, the single celled "Caulobacter" resembles a highly organized factory, with specific "machinery" regulating each step in the cell cycle to ensure that changes occur at developmentally appropriate times. DNA is copied once per cycle by a particular group of molecules. Once a single DNA copy is placed in each

neg: Virus viruses have evolved mechanisms that inject their genome into the bacterial cell across the cell wall, while the viral capsid remains outside. Uncoating is a process in which the viral capsid is removed: This may be by degradation by viral enzymes or host enzymes or by simple dissociation; the end-result is the releasing of the viral genomic nucleic acid. Replication of viruses involves primarily multiplication of the genome. Replication involves synthesis of viral messenger RNA (mRNA) from "early" genes (with exceptions for positive sense RNA viruses), viral protein synthesis, possible assembly of viral proteins, then viral genome replication mediated by

neg: Synthetic replication Synthetic replication Synthetic replication was first introduced in Europe in 2001. Synthetic replication is done through a type of exchange traded fund (ETF). An important attribute of this specific type of fund is that it does not hold any underlying securities featured on its benchmark. Instead of holding these securities synthetic ETF’s use derivatives such as swaps to track the underlying index in the process of replication. In replication of these synthetic accounts the return is 100% tied to the ETF it represents. Therefore, the ETF “replicates” the fund’s it is tied to performance. In this process the ETF manager

neg: Replication (computing) these commands to another process, generally over a network to a different machine, which will mimic the operations of the source machine. Like block-level storage replication, the file-level replication allows both synchronous and asynchronous modes. In synchronous mode, write operations on the source machine are held and not allowed to occur until the destination machine has acknowledged the successful replication. Synchronous mode is less common with file replication products although a few solutions exist. File-level replication solutions allow for informed decisions about replication based on the location and type of the file. For example, temporary files or parts of a

neg: Synthetic replication be if you went to a bank and purchased a synthetic ETF for the purpose of replication. That fund may represent a certain group of stocks in Apple. However, the synthetic ETF is in no way physically attached to Apples stock. The bank you purchased the fund from would largely mirror Apples stock performance 100% through the use of derivatives and swaps in the process of replication and would charge you a fee for it. This is an extremely simple example but does describe the base process of synthetic replication. Synthetic replication Synthetic replication was first introduced in Europe in

neg: Cyanophages it becomes damaged. The virus up-regulates photosynthesis, which leads to an increased rate of D1 protein degradation, the host cell alone can not efficiently replace these proteins so the cyanophage replaces them for the host cell, allowing it to continue providing energy for the cyanophage replication cycle. It is evident that cyanophage replication is heavily dependent on the diel cycle. The first step in the infectious cycle is for the cyanophage to make contact and bind to the cyanobacteria, this adsorption process is heavily dependent on light intensity. Field studies also show that the infection and replication of cyanophages is