Answer:
B) a nonsense mutation; this is because a nonsense mutation results in the change of a regular amino acid codon into a stop codon, which ceases translation. This fits with the problem's description of the protein that causes the symptoms as too short, as translation is the process by which proteins/polypeptides are created. A missense mutation would not be the answer because it still codes for an amino acid, which would not shorten the protein. A duplication of the gene would probably just lengthen the protein or not affect its length at all.
<span>More individuals are produced each generation that can survive.
Phenotypic variation exists among individuals and the variation is heritable.
Those individuals with heritable traits better suited to the environment will survive.
<span>
When reproductive isolation occurs new species will form.</span></span>
Answer:
d. Ribosome
f. Cell wall
Explanation:
In humans 80s type of ribosome is present and in bacteria 70s type of ribosome is present. Human cells do not have cell wall while bacterial cells have peptidoglycan cell wall. These differences can be targeted by the potential antibacterial agents.
For example, tetracycline antibiotic inhibits the binding of important molecules to bacterial ribosome which ultimately inhibits the protein synthesis in bacteria. Vancomycin antibiotic on other hand inhibits the cell wall formation in bacteria by inhibiting peptidoglycan synthesis.
