The correct answer is the last statement.
If the regulatory serine is mutated to alanine, then acetyl-CoA carboxylase will get activated spontaneously and will produce malonyl-CoA. The increased concentrations of malonyl-CoA will obstruct the oxidation of fatty acids by preventing the entry of fatty acids into the mitochondria.
It is because the AMP-activated protein kinase phosphorylates the serine residues of acetyl-CoA carboxylase to inactivate it. If a mutation occurs in such residues, then the AMPL cannot phosphorylate acetyl-CoA carboxylase and this enzyme will get activated spontaneously.
In such a situation, there will be more than sufficient production of malonyl-CoA, which will inhibit the admittance of more fatty acid getting inside the mitochondria; this will indirectly prevent the oxidation of fatty acids.
Choose and pick may be an example
In prokaryotes the 5' UTR is 3-10 nucleotides.
In Eukaryotes the 5'UTR is 100 to many thousand nucleotides long.
Explanation:
Leader sequence or 5' UTR starts at transcription site and ends at the initiation codon just one nucleotide away from it.
It is present in mRNA.
These are GC rich and form secondary structure, helps in protein synthesis.
Shine Dalgarno sequence in prokaryotes is an example of 5'UTR.
It acts as an entry point of ribosome.
Number 1 is B and number 2 is C.
