Answer:
Explanation:
The human ear is the organ for hearing. It converts sound waves into electrical impulses through which the brain processes to facilitate our hearing.
The ossicles inside the ear amplify sound waves they collect from the environment and transmits them into the inner ear.
Once in the inner ear, they are converted into electrical signals the brain can easily understand and discern.
Answer:
The correct answer would be - MMR would be hindered because both strands would be unmethylated and both would appear as new DNA strands and it would not be able to determine which strand has the error
.
Explanation:
In gene expression or DNA replication, the enzyme responsible for the synthesis of DNA from nucleoside triphosphate causes errors sometimes such as mismatch base pair that result in a change in genetic makeup.
For MMR, the DNA template and the strand formed required easily to be differentiated. As the newly synthesized strand is unmethylated and the DNA template strand is methylated results in DNA remain hemimethylated for a very short period.
After MMR, DNA adenine methylase enzyme that transfers a methyl group to the adenine of the sequence 5'-GATC-3' daughter strand formed.
Mutated DAM or DNA adenine methylase will not be able to transfer methyl group which leaves both template and daughter strands unmethylated and mismatch repair would be hindered as it will not be able to identify.
The resulting compounds of glycolysis can undergo other Adenosine triphosphate (ATP) to produce more ATP in the cell.
<h3>
What is glycolysis?</h3>
Glycolysis is a process in which glucose is partially broken down by cells in enzyme reactions that do not need oxygen.
Glycolysis is one method that cells use to produce energy.
<h3>Resulting compounds of glycolysis</h3>
During glycolysis, glucose ultimately breaks down into pyruvate and energy.
Thus, the resulting compounds of glycolysis can undergo other Adenosine triphosphate (ATP) to produce more ATP in the cell.
Learn more about glycolysis here: brainly.com/question/1966268
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