Note that both the initial GCT and the final GCG code for alanine; because of the degenerate coding mentioned above, there are four codes for alanine in the standard genetic code.
Most mRNA has a terminating poly-A tail. This terminal sequence makes it easy to pick out the labeling reactions that are used before hybridization to DNA microarrays, described in section 3.1.
Processing of amino acid chains Once the protein is formed, it has to find the right place to perform its function, whether as a structural protein in the cytoskeleton, or as a cell membrane receptor, or as a hormone that is to be secreted by the cell. There is a complex cellular apparatus that determines this translocation process. One of the determinants of the location and handling of a polypeptide is a portion of the polypeptide called the signal peptide. This header of amino acids is recognized by the translocation machinery and directs the ribosomal-mRNA complex to continue translation in a specific subcellular location, e.g., constructing and inserting a protein into the endoplasmic reticulum for further processing and secretion by the cell. Alternatively, particular proteins may be delivered after translation and chaperones can prevent proper folding until the protein reaches its correct destination.
Transcriptional programs Initiation of the transcription process can be caused by external events or by a programmed event within the cell. For instance, the piezoelectric forces generated in bones through walking can gradually stimulate osteoblastic and osteoclastic transcriptional activity to cause bone remodeling. Similarly, heat shock or stress to the cell can cause rapid change or initiation of the transcriptional program. Additionally, changes in the microenvironment around the cell, such as the appearance of new micro- or macronutrients or the disappearance of these, will cause changes in the transcriptional program. Hormones secreted from distant organs bind to receptors which then directly or indirectly trigger a change in the transcriptional process.
There are also fully autonomous, internally programmed sequences of transcriptional expression. A classic example of this is the internal pacemaker that has been found with the clock and per genes (see figure 1.8 below) where, in the absence of any external stimuli, there is a recurring periodic pattern of transcriptional activity. Although this rhythmic pattern of transcription can be altered by external stimuli, nonetheless it will continue initiating this pattern of transcription without any additional stimuli.
Figure 1.8: Genetic machinery of the circadian rhythm. Current molecular model of rhythm generation in Drosophila, from . The succession of events (A-F) occur over the course of approximately 24 hours. A, CLOCKBMAL heterodimers bind the per and tim promoters and activate mRNA expression from each locus; CLOCKBMAL may also activate transcription of other circadian-regulated genes (not shown). B, per and tim mRNA are transported to the cytoplasm and translated into PER and TIM protein, respectively. C, Regulation of protein levels occurs by two mechanisms: DBT protein phosphorylates and destabilizes PER, and light destroys TIM. Light during the early subjective night can phase-delay the clock. Small "blobs" indicate degraded proteins. D, PER and TIM levels slowly accumulate during the early subjective night; TIM stabilizes PER and promotes nuclear transport. E, PER and TIM dimers enter the nucleus and inhibit CLOCKBMAL-activated transcription. F, Protein turnover (combined with the lack of new PER and TIM synthesis) leads to derepression of per and tim mRNA expression; the cycle begins again (A). Light during the late subjective night can phase-advance the clock.
Finally, there are pathological internal derangements of the cell which can lead to transcriptional activity. Self-repair or damage-detection programs may be internal to the cell, and can trigger self-destruction (called apoptosis) under certain conditions, such as irreparable DNA damage. As another example, there may be a deletion mutation of a repressor gene causing the gene normally repressed to instead be highly active. There are many clinical instances of such disorders, such as familial male precocious puberty  where puberty starts at infancy due to a mutation in the luteinizing hormone receptor. This receptor normally activates only when luteinizing hormone is bound, but with the mutation present, activation does not require binding.
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