This question is asking about alternative splicing. Alternative splicing is a means by which several different proteins can arise from the same pre-mRNA due to the order in which the exons are organized. This typically takes the form of exon skipping. Therefore, both 1 and 2 are potential mature mRNAs that could arise from this pre-mRNA. Option 3 is not an acceptable transcript, however, because alternative splicing maintains the integrity of the genomic order of the exons (i.e. exon 4 will not come before exon 1, 2, or 3).

After transcription, the resulting RNA molecule must undergo post-transcriptional modification before it becomes mature mRNA. Before these modifications, it is known as heteronuclear RNA (htRNA) or pre-mRNA.

Introns are portions of pre-mRNA molecules that are spliced prior to translation. Unlike exons, introns do not contain information about the structure of the protein. Only after intron splicing is the molecule considered mRNA.

Immediately following transcription, the primary transcript will undergo a variety of changes before being translated. One of the largest changes is that a spliceosome complex will remove introns from the primary transcript. Introns are not involved in protein creation, and their removal makes the transcript much shorter. The final mRNA transcript consists of a string of exons, a 5' cap, and a 3' poly-A tail.

These are all reasons that introns are important, despite the fact that they are not included in final proteins. Introns can allow for alternative splicing of exons, in which exons are placed in different orders to create different proteins from one gene. In the gene Dscam in Drosophila, alternative splicing allows for around 38,000 different proteins from one gene sequence. Some introns become non-coding RNAs that control expression of genes. Lastly, it has recently been shown that introns are involved in some special functions like mRNA export - in which mRNA's are moved between the nucleus and other cellular compartments.

The primary RNA contains introns and exons because it has not been processed yet, and therefore the introns have not been spliced out. Mature mRNA contains only exons, which are the coding sequences that ultimately get translated. Intron regions are non-coding and are not included in mature transcripts. Note that post-translational modifications such as splicing only occurs in eukaryotes.

This question requires you to know that preRNA contains both intronic and exonic regions, but the introns get spliced out to produce the mRNA. Therefore, you had to subtract the total intron basepairs (250) from the total length of the preRNA (1200), which gives an mRNA length of 950 basepairs. 

The promoter is a specific segment of DNA that signals the starting point of transcription. RNA polymerase attaches to the promoter and proceeds to create the mRNA primary transcript.

DNA polymerase binds to the RNA primer to begin DNA replication. Ribosomes bind to the 5' cap on eukaryotic mRNA.

The important thing to remember about the lac operon is that it is transcribed when glucose is absent from the cell, but lactose is present and can be utilized. As a result, the operon's transcription would be high if there are both high levels of lactose available, and very little amounts of glucose.

The lac operon is set up in a way so that the lac repressor is able to be transcribed, regardless of glucose and lactose levels. The lac repressor will then attach to the operator, which inhibits transcription. If lactose is present, it will bind to the lac repressor, and make it detach from the operator.

This process allows the operon to be transcribed in the event that glucose is absent. If glucose is absent, but lactose is not present, then the repressor will remain in place and transcription will not take place.

The question informs us that the mutational defect in the gene involves the enzyme's ability to load copper onto apoceruloplasmin. Healthy individuals are able to load copper to apoceruloplasmin, creating serum-soluble ceruloplasmin. With this process disrupted in an individual with Wilson's Disease, we would expect that less ceruloplasmin would be produced because copper could not be transported. We would expect to see reduced serum levels of the complete protein, and high levels of copper building up in hepatocytes and circulatory serum.