Post-transcriptional control of protein synthesis

Evidence for Post-Transcriptional Control of Protein Synthesis in Animal Cells. 191... 

Post-transcriptional control of protein synthesis in bacteria seems to be confined to the possible existence of messenger or cistron-specific initiation factors and their modification after phage infection. In animal cells, however, where the site of transcription is physically separated by the nuclear membrane from the protein synthesizing apparatus in the cytoplasm, there is die possibility of more complex forms of control, and some of these will be discussed lielow. 

Indeed, inhibitors of protein synthesis have been used in the in vivo rabbit [60] and in the rat LangendorfT models [61]. Cycloheximide or actinomycin D did not reverse the PC effect [60]. This is probably due to non-complete inhibition of protein synthesis. The latter study [61] showed that the PC effect was abolished only with cycloheximide, but not with actinomycin D, indicating that PC protection is regulated at the post-transcriptional level. Recent findings [62] have reconfirmed the translational control of protein synthesis in ischemic (but not pharmacological) PC. These are in accord with our findings concerning de novo synthesis of ferritin. 

Chloroplast protein synthesis is controlled largely at the post-transcriptional level [20,21] and can be repressed by the inclusion of antibiotics such as streptomycin in the sprouting medium. Streptomycin binds to the 16S rRNA and causes the ribosome to misread the mRNA sequence, producing incorrect and non-functional proteins [22]. 

Though still scanty and incomplete, the data indicate that the control of synthesis of enzymes participating in secondary biosynthesis is accomplished at the transcription level. Their formation takes place after a reduction in the rate of RNA and protein syntheses. The period of intensive secondary biosynthesis is marked by the continuous replenishment of specific synthases its discontinuation brings about a drop in the production rate. The "late" expression of synthesis of secondary metabolites after the termination of intensive growth is thus probably not the result of a post-translation control (23, 24). So far, we cannot eliminate a number of other control mechanisms at the level of activity of the enzymes formed, yet the rise in synthase levels in the period of active secondary biosynthesis (4, 30, 38) attests to our hypothesis. 

Ascorbate transport is mainly controlled by carriers availability, and thus it depends on the number of SVCT proteins present in the plasma membrane (which in turn is related to enhanced synthesis, slowed degradation, activation of nonfunctional carriers or cellular redistribution), as well as their substrate affinity. So, transcriptional, translational, and post-translational modifications of SVCTs allow a fine-tuned regulation of AA uptake (Liang et al., 2002). 

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