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Multiplicity of Infection
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M u l t i p l i c i t y o f I n f ection
types. Normally, it is stimulated by binding a circulating ligand molecule and a cell surface co-receptor. The RET mutations in MEN 2 are almost exclusively single amino acid substitutions that result in continuous, unregulated activation of the RET receptor. Unlike those found in other cancer syndromes, MEN 2 mutations do not inactivate RET but either render it independent of the ligand molecules that normally control its activity or cause RET to recognize inappropriate targets that trigger a cascade of interactions leading to cell proliferation. More than 95% of MEN 2 patients inherit a mutation that changes one of only 10 amino acids in the protein, making mutation testing in MEN 2 quite simple to perform. Once a RET mutation is identified, the patient generally undergoes prophylactic surgery to remove the thyroid before tumors can arise, effectively removing the major tumor risk. Thus, MEN 2 represents an instance where identification of the disease causing mutation has greatly improved our ability to both diagnose and manage the disease.
to initiate an infection, the zero-order term of the Poisson distribution can be used to calculate the actual MOI of infecting phage particles, given the number of surviving (i.e., uninfected) bacteria. This calculation makes the assumption that all parts of the culture were equally accessible to the bacteria and phage, i.e., that the two were thoroughly mixed: No: of surviving bacteria e original bacterial titer
MOI
Thus, the MOI ln (fraction of bacteria that survive the infection). When carrying out genetic crosses, the relative numbers of each of the two different phages involved can be calculated by using the appropriate term of the Poisson distribution. Such techniques are discussed in Karam (1994).
Reference
See also: RET Proto-Oncogene
Karam J (ed.) (1994) Molecular Biology of Bacteriophage T4, Washington, DC: American Society for Microbiology Press.
Multiplicity of Infection
See also: T Phages; Virulent Phage
E Thomas Copyright ß 2001 Academic Press doi: 10.1006/rwgn.2001.0858
Multisite Mutation R L Somerville
Multiplicity of infection (MOI) is the ratio between the number of viruses in an infection and the number of host cells. This ratio can be determined approximately by adjusting the relative concentration of virus and host. It cannot be determined exactly for each individual host cell, but the average MOI can be calculated. The ability to adjust this ratio is important. In some experiments it is important that there is only one virus infecting each host cell. In others, it is most important to ensure that virtually all host cells have been infected, possibly with each of two different phage mutants if genetic experiments are being conducted, and a high MOI is used. Both the phage and bacteria diffuse randomly and collide and bounce off each other until the phage interacts with an appropriate receptor. At any given average MOI, there will be a substantial range in the number of phage that infect each bacterium; a mathematical function called the `Poisson distribution' can be used to show the distribution in number of phage per cell at any given MOI. Some bacteria will not be infected at all, even at high MOI. For very virulent phage like T4, where a single phage particle is sufficient
Copyright ß 2001 Academic Press doi: 10.1006/rwgn.2001.0859
A multisite mutation is one of a category of permanent, heritable change in DNA that is the result of the loss of more than two adjacent nucleotide pairs from the genome. This type of mutation is also a deletion ± although not every deletion is a multisite mutation, because deletions of 1 bp can occur. The term `multisite' was coined prior to the advent of molecular techniques for DNA analysis, when pairwise crossing between mutant organisms was a prominent method for analyzing genome structure. Operationally speaking, multisite mutations were distinguished from `point' mutations by virtue of their inability to yield wild-type recombinants in pairwise crosses with more than one different point mutant. Mutants were classified as `point' if they could be shown to undergo true reversion; multisite mutations fail to revert (although sometimes they may be phenotypically reversed by suppressor mutations). There is no upper limit to the number of nucleotide pairs whose deletion can give
M u l t i p l i c i t y o f I n f ection
types. Normally, it is stimulated by binding a circulating ligand molecule and a cell surface co-receptor. The RET mutations in MEN 2 are almost exclusively single amino acid substitutions that result in continuous, unregulated activation of the RET receptor. Unlike those found in other cancer syndromes, MEN 2 mutations do not inactivate RET but either render it independent of the ligand molecules that normally control its activity or cause RET to recognize inappropriate targets that trigger a cascade of interactions leading to cell proliferation. More than 95% of MEN 2 patients inherit a mutation that changes one of only 10 amino acids in the protein, making mutation testing in MEN 2 quite simple to perform. Once a RET mutation is identified, the patient generally undergoes prophylactic surgery to remove the thyroid before tumors can arise, effectively removing the major tumor risk. Thus, MEN 2 represents an instance where identification of the disease causing mutation has greatly improved our ability to both diagnose and manage the disease.
to initiate an infection, the zero-order term of the Poisson distribution can be used to calculate the actual MOI of infecting phage particles, given the number of surviving (i.e., uninfected) bacteria. This calculation makes the assumption that all parts of the culture were equally accessible to the bacteria and phage, i.e., that the two were thoroughly mixed: No: of surviving bacteria e original bacterial titer
MOI
Thus, the MOI ln (fraction of bacteria that survive the infection). When carrying out genetic crosses, the relative numbers of each of the two different phages involved can be calculated by using the appropriate term of the Poisson distribution. Such techniques are discussed in Karam (1994).
Reference
See also: RET Proto-Oncogene
Karam J (ed.) (1994) Molecular Biology of Bacteriophage T4, Washington, DC: American Society for Microbiology Press.
Multiplicity of Infection
See also: T Phages; Virulent Phage
E Thomas Copyright ß 2001 Academic Press doi: 10.1006/rwgn.2001.0858
Multisite Mutation R L Somerville
Multiplicity of infection (MOI) is the ratio between the number of viruses in an infection and the number of host cells. This ratio can be determined approximately by adjusting the relative concentration of virus and host. It cannot be determined exactly for each individual host cell, but the average MOI can be calculated. The ability to adjust this ratio is important. In some experiments it is important that there is only one virus infecting each host cell. In others, it is most important to ensure that virtually all host cells have been infected, possibly with each of two different phage mutants if genetic experiments are being conducted, and a high MOI is used. Both the phage and bacteria diffuse randomly and collide and bounce off each other until the phage interacts with an appropriate receptor. At any given average MOI, there will be a substantial range in the number of phage that infect each bacterium; a mathematical function called the `Poisson distribution' can be used to show the distribution in number of phage per cell at any given MOI. Some bacteria will not be infected at all, even at high MOI. For very virulent phage like T4, where a single phage particle is sufficient
Copyright ß 2001 Academic Press doi: 10.1006/rwgn.2001.0859
A multisite mutation is one of a category of permanent, heritable change in DNA that is the result of the loss of more than two adjacent nucleotide pairs from the genome. This type of mutation is also a deletion ± although not every deletion is a multisite mutation, because deletions of 1 bp can occur. The term `multisite' was coined prior to the advent of molecular techniques for DNA analysis, when pairwise crossing between mutant organisms was a prominent method for analyzing genome structure. Operationally speaking, multisite mutations were distinguished from `point' mutations by virtue of their inability to yield wild-type recombinants in pairwise crosses with more than one different point mutant. Mutants were classified as `point' if they could be shown to undergo true reversion; multisite mutations fail to revert (although sometimes they may be phenotypically reversed by suppressor mutations). There is no upper limit to the number of nucleotide pairs whose deletion can give