Individuals with Turners Syndrome have the XO genotype. They are phenotypically female but experience abnormalities. XXY is the genotype of an individual with Klinefelter syndrome. Individuals with the genotype XYY have what is known as XYY syndrome and are phenotypically normal, though they may be taller, and secrete excess testosterone. Triple-X syndrome is cause by an XXX genotype, and individuals are phenotypically normal. Lack of an X chromosome is lethal in humans.

Individuals with Turners Syndrome have the XO genotype. They are phenotypically female but experience abnormalities. XXY is the genotype of an individual with Klinefelter syndrome. Individuals with the genotype XYY have what is known as XYY syndrome and are phenotypically normal, though they may be taller, and secrete excess testosterone. Triple-X syndrome is cause by an XXX genotype, and individuals are phenotypically normal. Lack of an X chromosome is lethal in humans.

Recombination between homologous chromosomes is one of the only methods for repairing double-stranded breaks in DNA without losing information. This method only works, however, if there is an extra copy of the same DNA in the cell (i.e. on a homologous chromosome). Recombination is not possible prior to the S phase of the cell cycle, during which DNA is replicated.

Non-homologous end joining results in the deletion of a few base pairs, which can be problematic if done in the coding region of a gene. Translesion synthesis actually has nothing to do with double-stranded breaks, and refers to a method of accurately synthesizing DNA over mutations (such as thymine dimers) by using specialized polymerases.

Recombination between homologous chromosomes is one of the only methods for repairing double-stranded breaks in DNA without losing information. This method only works, however, if there is an extra copy of the same DNA in the cell (i.e. on a homologous chromosome). Recombination is not possible prior to the S phase of the cell cycle, during which DNA is replicated.

Non-homologous end joining results in the deletion of a few base pairs, which can be problematic if done in the coding region of a gene. Translesion synthesis actually has nothing to do with double-stranded breaks, and refers to a method of accurately synthesizing DNA over mutations (such as thymine dimers) by using specialized polymerases.

The correct answer is linkage disequilibrium. This phenomenon occurs when two alleles do not segregate independently even though they are at different loci. Rather, they are statistically associated with one another above non-random conditions. This is important for understanding evolution of organisms from a common ancestor as well as for identification of disease-associated mutations or single nucleotide polymorphisms.

The correct answer is linkage disequilibrium. This phenomenon occurs when two alleles do not segregate independently even though they are at different loci. Rather, they are statistically associated with one another above non-random conditions. This is important for understanding evolution of organisms from a common ancestor as well as for identification of disease-associated mutations or single nucleotide polymorphisms.

The correct answer is mosaicism. Mosaicism within an organism occurs when mutations, such as non-disjunction, occur in a subset of cells to give rise to genetically distinct cell populations. Chimeras also have genetically distinct cell populations, however, they occur from the fusion of two fertilized embryos. Aneuploidy occurs when an organism has an incorrect, but consistent number of chromosomes.

The correct answer is mosaicism. Mosaicism within an organism occurs when mutations, such as non-disjunction, occur in a subset of cells to give rise to genetically distinct cell populations. Chimeras also have genetically distinct cell populations, however, they occur from the fusion of two fertilized embryos. Aneuploidy occurs when an organism has an incorrect, but consistent number of chromosomes.

This question is somewhat vague because we are given no other information other than the fact that there is a "mutation". Mutations can take many different forms and, therefore, we would need to know more information about the specific type of mutation before we can say whether or not the plasmid still contains a functional gene for the wild type protein. In particular, a silent mutation would result in the insertion of the exact same amino acid despite having a different codon (this is due to the redundancy of the genetic code). If a silent mutation has altered the sequence of the plasmid, it will not alter the structure or function of the protein and the plasmid will still be effective.

A frameshift mutation, however, would have disastrous effects on the protein as the translational reading frame would be shifted and the protein would most likely be truncated and nonfunctional.

This question is somewhat vague because we are given no other information other than the fact that there is a "mutation". Mutations can take many different forms and, therefore, we would need to know more information about the specific type of mutation before we can say whether or not the plasmid still contains a functional gene for the wild type protein. In particular, a silent mutation would result in the insertion of the exact same amino acid despite having a different codon (this is due to the redundancy of the genetic code). If a silent mutation has altered the sequence of the plasmid, it will not alter the structure or function of the protein and the plasmid will still be effective.

A frameshift mutation, however, would have disastrous effects on the protein as the translational reading frame would be shifted and the protein would most likely be truncated and nonfunctional.