BIOLOGY:BRIEFLY explain how gene expression is controlled during and after translation?

A-T/U
C-G.

Whatever order the neucleotides come in, the groups of 3 (codons) will determine which amino acids are made. Therefore causing proteins to be made and/or gene expression to be shown.

Example NOT ACCURATE:
 GTA -> Aminoacidite -> Prototienipe -> Blue eyes.



If a shifting mutation occurs, the whole sequence after the mutation will get all screwed up because of the whole line moving down 1-3 places. Its like a zipper, one little mistake and it won't go back together correctly. More than likely, the protein for stopping cell growth will be affected (causing cancer).
If a point mutation (meaning just one or two mistakes) occurs, It is very unlikely that cancer will develop, but it can still happen. I know that if you have an insertion or deletion mutation, it can cause as much damage as the whole shift. Thats why point mutations are the least likely to cause damage.

During translation:
Gene expression is controlled by proteins that bound to mRNA's that will control whether or not the gene is actually translated. Whether or not the gene is translated determines whether or not the gene is expressed. If regulatory proteins direct the mRNA's to the ribosome, then the genes will be translated and thus expressed. (mutations CAN occur here, but that's not something the gene itself can control, as it is an error in translation).

After Translation:
Gene expression is controlled here through chemical modification of the protein product made during translation. After the protein product is made, it can be tagged by proteins such as ubiquitin. If the proteins are mutated or misfolded, ubiqutin will send the error-protein to the proteasome. Proteins can also be inactivated or activated by phosphorylation, which can constitute whether or not a gene is expressed.

Cancer Question:
Well, there are two ways cancers can occur. Proto-oncogenes could be mutated into oncogenes, and tumor suppressors could be mutated in a way that they can't do their jobs.

Proto-oncogenes promote cell division: if they are mutated, then cells (good or bad) will divide uncontrollably, hence cancer. Proto-oncogenes can be mutated the same way other genes are mutated: point mutations or deletions, or something happens that causes hyper-expression of the proto-oncogene product. An example of this are MPFs (mitotic promoting factors), found in the G1 stage of the cell cycle.

Tumor Suppressors are genes that STOP the cell cycle. Meaning, it prevents cells from dividing. If these are mutated, obviously they can't do their job (stop cells from dividing) which leads cells to divide uncontrollably, causing cancer. An example of this is the p53 gene, which triggers apoptosis (cell suicide).