The ability of a gene to affect an organism is multiple ways is called pleiotropy. During post-transcriptional modification, introns are removed from the mRNA sequence and exons are spliced together to create the desired protein product. By splicing the gene in different ways, different proteins can be produced, which will affect different traits.

Consider the sentence: The man ran on the track, but fell.

By splicing different portions of the sentence, it can take on different meanings: The man ran. The man on the track fell. The man fell. The man ran, but fell.

Where pleiotropic genes affect more than one trait, polygenic traits are affected by multiple genes. Epistatic genes are regulated by the activation of other genes.

Out of the choices, only methylation of histones is commonly associated with the silencing of genes. Proteins known as histone methyltransferases bind a methyl group to amino acids in the histone, most commonly lysine or arginine. The result is a change in chromatin structure, most commonly blocking transcription sites and preventing expression.

Acetylation of histones is often found in activated genes. Phosphorylation of histones has been seen in DNA regulation, but it is unclear whether or not this modification affects the expression of genes.

Topoisomerases unwind supercoiling of DNA by breaking and rejoining DNA chains. 

Nucleotide excision repair (NER) is used to repair thymine dimers, which are caused by ultraviolet damage. It also repairs bulky DNA adducts caused by carcinogens.

DNA polymerase III has these two functions:

1. 5'-3' polymerase requiring a 3' hydroxide primer and a DNA template

2. 3'-5' exonuclease proofreading

Both DNA polymerase I and DNA polymerase III are prokaryotic only. DNA polymerase I excises RNA primers with a 5' to 3' exonuclease.

5'-3' exonuclease removal of primers by DNA polymerase I.

DNA polymerase I is prokaryotic only, it degrades RNA primer and fills in the gap with DNA.

Base excision repair (BER) requires glycosylases.

BER steps:

1. Glycosylases recognize incorrectly paired or damaged bases and 'flip' them out of the DNA chain without disrupting the phosphodiester backbone. The N-glycosidic bond of the flipped base is cleaved, leaving an AP site (site without a base).

2. AP site is removed by AP endonucleases and an AP lyase.

3. DNA polymerase I (prokaryotes) or DNA polymerase beta (humans) replaces the gap with a new base and DNA ligase seals the strand.

DNA control elements are contained within the DNA helix.

DNA control elements:

1. TATA box: 25-35 basepairs (bps) upstream from start site, determines site of transcription and directs RNA polymerase II binding

2. Proximal promoter elements: 200 bps upstream of start and are roughly 20bps long

3. Enhancers are short regions of DNA that can be 50-1500bp long. They can be bound by activators to increase transcription. Can be far from the site of transcription and still be functional

NOT DNA control elements:

Transcription factors: bind to DNA control elements to influence transcription but are not considered control elements themselves.

Transcriptional repressors and activators: proteins coded by one gene that act to regulate transcription

Ultraviolet light causes thymine dimers in DNA. 

Alternative splicing can:

1. Retain/remove exons.

2. Retain/remove introns.

3. Truncate/extend at 5' or 3' ends.

4. Have mutually exclusive exons (one or the other, but never both).