Trying to understand this/connect the micro to the macro.
We know that there is differential gene expression.
This could be caused by environmental factors activating/repressing differnet protein cascades which in turn activate or repress different genes.
But on the level of the promoters themselves, how can you have tissue specific promoters if teh DNA Is the same in every cell?
For the purpose of the MCAT, you should understand that the distinction between different cell types ultimately is due to differential gene activation/silencing (during development) and gene expression (within a given cell). Although each cell type has the same DNA in its nucleus, during the developmental process (beginning at gastrulation), several of the genes contained within the DNA are permanently silenced (turned off), while others remain active (turned on). This occurs variably for different cells. The expressions of these genes and their associated products (proteins) ultimately produce the unique cell characteristics (phenotype). However you should also realize that although any two given cells, for instance a neuron and a cardiac muscle cell, have certain active genes exclusive to each cell type -- there is also some overlapping genes that they both share which are necessary for fundamental processes such as metabolism and energy production pathways.
The whole dynamic of how this occurs is a bit complicated and something that I personally don't have too much experience with. From what I recall, an early colony of embryonic stem cells (inner mass of the blastocyst) begin releasing certain 'chemicals' called inducers which stimulate changes within neighboring cells, specifically the activation and silencing of genes mentioned above. There are many ways this silencing can occur. One example I am aware of is the process of methylating bases of DNA, particularly cytosine. It has been demonstrated experimentally that variations in methylation alter gene expression: low 5'-mC is associated with high gene expression and vice versa; additionally, this modification has been shown to be heritable from generation to generation (cell lines). Also, the methylation pattern itself appears to be tissue specific, which is expected if only a subset of all the genes in the genome are to be expressed in a single tissue type. This seems to fall in line with the idea that, during the specialization process, cells are first determined (that is, destined for one particularly pathway) followed by differentiation (additional specialization based on variation of gene expression).
It's worth noting that although a given specialized cell can have many different genes, the rate of expression of each gene product is highly regulated by environmental stimuli and other internal factors all interacting with one another. Certain pathways might for instance, activate a group of transcription factors which bind to the promoter region and alters the transcription rate of a certain gene product to be transcribed and eventually translated. But it's really much more complicated than that because you have to consider different levels of regulation too (aside from differential expression of active genes). Alternative splicing of mRNA produces many variants of a given gene (which disproves the common notion that one gene = one product). Moreover, the actual mRNA product varies in stability (ie. can be influenced by length of poly-A tail; other non-coding RNA alter stability: miRNA - these bind to complementary DNA sequences, blocking translation and promoting destruction). Or, the protein that was translated can be readily degraded at different rates (ie. ubiquitin tagging for destruction). FYI - I only mention these examples because it has been commonly presented in past MCAT exams (miRNA and it's associated activity in relation to its effect on cancer). Anyways, as I said before, it's really complicated but as long as you have a general understanding of this, I think you'll be okay. Hope this answers your question and clears any confusion.
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One very interesting thing to mention is regarding B cell development (a very unique feature). All of these cells originate from a common stem cell, so how then is it possible for us to have so many varieties of B cells in our body, each with a unique surfice immunoglobin for a specific antigen? Well, as it turns out - the stem cell has multiple gene segments encoding portions of a single immunoglobulin heavy or light chain. During B-cell maturation in the bone marrow, these gene segments are randomly shuffled by a dynamic genetic system capable of generating more than a million different combinations. But it doesn't end there! Additional modifications produces even more unique combinations, accounting for the billions of antigenic variations we can detect. This diversity is so important and is one of the primary mechanisms we evolved to protect us from foreign invaders. I know my nerdiness is showing here, but it really blows my mind. If you ever get an opportunity to take an upper level immunology course before Medical School, definitely do it. Your whole perspective of Biology and Medicine will change and you'll have a much greater appreciation for the subject.
EDITTED: for grammar, some added clarity, and cool info
