This question is inspired by a real life example, in which if you put a bat enhancer region in front of the gene that controls limb development in mice, the limbs are longer due to changes in the enhancer activity, which increases the activity of the promoter. By permitting more transcription factor interaction with the regulatory region, one might expect that this type of mutation may increase the tail length of the mouse because more "pro-tail length" protein is being made.

The correct answer is to promote formation of euchromatin and increase gene expression. Acetylation of histones "relaxes" DNA coiling around histones by reducing the affinity between histones and DNA. This allows transcription factors to bind promoter regions and promote increased gene expression via transcription.

The correct answer is that mediator is a coactivator of transcription and serves to recruit transcription factors and RNA polymerase II. Mediator does not directly initiate transcription; however, by protein-protein interactions, it recruits the necessary proteins to sites of transcription. 

Upstream signaling, such as from a toll-like receptor, causes IKK to phosphorylate IkB, signaling for its ubiquitin-mediated degradation. Since NFkB is no longer bound by its inhibitor, IkB, it translocates to the nucleus where it binds specific motifs in the genome to recruit other transcriptional machinery and initiate transcription. 

The correct answer is recruiting DNA polymerase. DNA polymerase is involved in DNA replication, not transcription. Pioneer transcription factors can bind specific DNA motifs and promote euchromatin formation, allowing other transcription factors to bind the less organized DNA. Transcription factors can recruit other transcription factors and the RNA polymerase holoenzyme to promoters to promote gene-specific transcription. 

Protein synthesis can be directly affected by molecules involved in translation, or indirectly by molecules involved in the transcription of mRNA templates.

Transfer RNA (tRNA) is involved in translation and serves the function of bringing amino acids to ribosomes. Due to its important function in translation tRNA, is capable of globally controlling translation and, therefore, is involved in protein regulation.

Long non-coding RNA (lncRNA) has been shown to regulate transcription in a number of ways. One of the most prominent is the existence of a lncRNA (Xist) that inactivates the majority of the extra X-chromosome in human females.

Micro RNA (miRNA) is involved in a process known as RNAi and is capable of controlling the translation of targeted molecules of mRNA. 

The correct answer is long non-coding (lnc) RNA. Xist lncRNA coats the X-chromosome from which it is transcribed, effectively silencing that X-chromosome. MicroRNAs are small RNAs (~20 base pairs (bp)) and play a role in RNA silencing and post-transcriptional regulation of gene expression. Short interfering RNAs are double-stranded (20-25 bp) and play a role in post-transcriptional gene silencing. Piwi-interacting RNAs are small non-coding RNAs that interact with piwi proteins in epigenetic and post-transcriptional silencing of genetic elements such as retroposons. While MicroRNAs, siRNAs and Piwi-interacting RNAs all silence genes, the mechanism of X-chromosome inactivation requires Xist lncRNA. 

Synthetic lethality is the correct answer. The combinatorial effect of multiple mutated genes disrupts homeostasis in cells, inducing cell death. A mutation in only one gene can be compensated for in cells by altering the expression of other genes, such as turning on anti-apoptotic signaling pathways. 

Oncogene addiction occurs when a tumor cell relies on the expression of a particular oncogene (mutated gene) for survival. 

Oncogenic shock refers to an increase in pro-apoptotic signaling and a decrease in anti-apoptotic signaling upon removal of an oncoprotein. 

Apoptosis refers to the process of programmed cell death. 

Secondary mutations occur in a cancer cell that is treated with a therapeutic agent to promote resistance to that specific agent. 

Histones are almost always modified on lysines. Acetylation normally is an activating mark, and methylation is normally a repressing mark of chromatin structure.

Note that guanine is not an amino acid, but a nucleotide. 

The correct answer is all of the other answers are correct. H3K4me1 (Histone 3 Lysine 4 methyl 1) marks where enhancers are in the chromatin landscape. By further identifying H3K27Ac or H3K27Me3 marks on the same histone, we can determine whether the enhancer is active or inactive, respectively. A DNase 1 hypersensitivity assay will preferentially cut open chromatin, which often is indicative of enhancer regions in the chromatin landscape.