By Joris Winderickx, Peter M. Taylor
Cells of all residing organisms be capable to reply to altered dietary stipulations. they've got built mechanisms to experience nutrient availability and to provide applicable responses, which contain alterations in gene expression and the construction or degradation of definite enzymes and different proteins. in recent times, the knowledge of nutrient-induced sign transduction has tremendously complex and the rising photo is that nutrient signalling mechanisms have advanced early in evolution. This e-book presents particular presentation and comparability of the foremost dietary regulatory mechanisms in decrease in addition to larger eukaryotes, written through regarded specialists during this increasing box.
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Extra resources for Nutrient-Induced Responses in Eukaryotic Cells
2003). Thus, mammalian cells have additional mechanisms to regulate eIF2 in response to nutrients in addition to the GCN2 pathway. Such mechanisms may be important in enabling mammalian cells to react to amino acid deficiency before significant accumulation of uncharged tRNAs occurs, which might otherwise compromise translational fidelity (Proud 2002).
2000), which then phosphorylates eIF2α and inhibits translation initiation. Amino acid deprivation also increases eIF2α phosphorylation in mammalian cells and it is likely that the mammalian and yeast GCN2 proteins perform broadly similar roles, possibly including sensing of amino acid availability via the level of tRNA charging (Sood et al. 2000; Fernandez et al. 2002; Zhang et al. 2002). This matter is considered in detail in Chapters 5 and 7. Amino acid alcohols can inhibit amino acyl-tRNA synthetases and thus block tRNA charging.
Another 42 Christopher G. Proud, Harinder S. Hundal, and Peter M. Taylor mechanism by which uncharged tRNA may influence translation is through an inhibitory effect on the enzyme phosphofructokinase (observed to date only in vitro) (Rabinovitz 1995), which would lead to a reduction in intracellular fructose-(1,6)bisphosphate (an activator of eIF2B; (for review see Rabinovitz 1995; Kimball 2002) in parallel with activation of the GCN2 pathway. There is very little evidence to suggest that levels of tRNA charging also underlie control of the mTOR pathway.