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.
I think that the Risk assessment depends on medicine. Here's some extra details: the PROCESS by which HAZARD, exposure and risk are determined. The four steps of risk assessment are Hazard identification<span>Dose-response assessment
Exposure assessment
Risk characterization</span>
Answer: A because two of the same pairs are homologous
Oxidative phosphorylation requires a proton gradient.
- Cells use enzymes to oxidize foods in the metabolic pathway known as oxidative phosphorylation, electron transport-linked phosphorylation, or terminal oxidation, which releases chemical energy to create adenosine triphosphate.
- This happens inside mitochondria in eukaryotes. The majority of the energy required for biosynthesis, maintaining a healthy ion balance, and mechanical effort is provided by oxidative phosphorylation, which is the principal source of ATP in higher animals.
- A succession of proteins and electron carriers in the mitochondrial membrane, as well as the electron transport chain, are all involved in the process of oxidative phosphorylation.
learn more about Oxidative phosphorylation here: brainly.com/question/13254827
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