RNA polymerase II is the polymerase that catalyzes the synthesis of mRNA from a coding strand of DNA. Therefore, mRNA synthesis would be greatly affected by an inhibition of RNA polymerase II.

For this question, we need to consider how histone acetyltransferases affect histones. Then, we need to determine how these modified histones affects the expression of genes.

First, it's important to note that histones are proteins that mostly contain positive charges. As a result of this, histones are able to associate with DNA very well, since DNA contains a negatively charged backbone. When histones associate with DNA in this way, the DNA molecule becomes tightly coiled around the histones. In this tightly bound conformation, the collection of DNA and proteins are referred to as hererochromatin. What's more is that when the DNA is tightly bound like this, the transcription machinery in the cell is physically blocked from associating with genes. Thus, gene expression is lowered.

Histone acetyltransferases are enzymes that attach acetyl groups to the positively charged lysine residues that are part of histones. Remember, the positive charge of these lysine residues is what allows the histones to associate with the DNA. When acetyl groups are added, the positive charge on these histones becomes neutralized. As a result, the histones are no longer able to associate with the DNA. What this means is that the transcription machinery in the cell is now able to physically access the genes, allowing gene expression to increase.

RNA polymerase III catalyzes the synthesis of tRNA - RNA that is responsible for carrying amino acids during translation. So, synthesis of protein will be affected down the line, however the direct effect of an inhibition of RNA polymerase III would be the inability to create tRNA.

RNA polymerase travels down DNA beginning at the promoter site (could be TATA box or Hogness box in eukaryotes). It reads the DNA and synthesizes mRNA along the way, until it reaches a point where it reads the DNA and synthesizes a termination sequence. This notifies the RNA polymerase that it should end transcription of the gene.

Spliceosomes recognize the conserved sequence, GU, and splice just before those two nucleotides. They then continue onwards and when they recognize a pyrimidine followed by the nucleotides, AG, they splice again immediately after the AG. This is almost always conserved in introns to ensure proper splicing.

There are few differences between prokaryotes and eukaryotes in what concerns transcription. In prokaryotes there is only one RNA polymerase, while in eukaryotes there are three: I , II and III. In prokaryotes, both sigma factor and rho factor are required for transcription to occur, but not in eukaryotes. 

The DH subunit is a dehydratase, meaning it removes alcohol groups from carbon chains. If this subunit is mutated, the alcohol cannot be removed. 

-hydroxybutyrate dehydrogenase catalyzes the interconversion of the ketone bodies acetoacetate and -hydroxybutyrate, which are transported out of liver cells into the blood to be used as fuel by the rest of the body, particularly during times of starvation. -hydroxybutyrate dehydrogenase’s only coenzyme is . As for the other answers: the pyruvate dehydrogenase complex converts pyruvate into acetyl-CoA, the key connection between glycolysis and the citric acid cycle, and this process uses a number of co-factors, including , thiamine pyrophosphate, lipoamide (the protein-bound form of lipoic acid), and, of course, coenzyme A (to make acetyl-CoA). Pyruvate dehydrogenase uses  and  depending on the cell type.

Because acetyl-CoA Carboxylase (ACC) is directly responsible for synthesis of malonyl-CoA, inhibiting it would be the most targeted approach. Inhibiting acyl-CoA dehydrogenase or pyruvate dehydrogenase would decrease available acetyl-CoA to ACC by inhibiting beta-oxidation and conversion of pyruvate to acetyl-CoA, but this would have a large impact on other biosynthetic pathways as well, due to the ubiquity of acetyl-CoA.

The endogenous, not the exogenous, pathway, involves the transformation of VDLDs into LDLs. Meanwhile, the exogenous, not the endogenous, pathway, involves transforming chylomicrons into remnants. The apolipoprotein in plasma (transporting cholesterol to the liver) which is the major component of HDL is A1, not B100. Macrophages do indeed oxidize LDLs and transform themselves into the foam cells which indicate atherosclerosis. This is one of the reasons that LDL cholesterol levels can indicate atherosclerosis (which is associated with increased risk of heart attack or stroke).