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. 2016 Jan 6;6(1):4. doi: 10.3390/biom6010004

Figure 2.

Figure 2

A proposed mechanism of NR1 mRNA regulation in normal and chronic ethanol exposed fetal cortical neurons: The NR1 mRNA is localized in the rough endoplasmic reticulum (RER) irrespective of ethanol treatment [36]. The normal half-life of NR1 mRNA is ~15 h in cultured fetal cortical neurons (FCNs). Following chronic ethanol exposure, the half-life of NR1 mRNA increases to more than 24 h in FCNs [35]. One of the potential mechanisms that can explain increase in NR1 mRNA half-life is increased binding of GIIβ to NR1 mRNA as demonstrated previously by us [38,39]. Decline in ethanol concentration, e.g., ethanol withdrawal in chronic ethanol exposed FCNs, triggers post-translational modification, e.g., phosphorylation of GIIβ—a process that occurs in normal FCNs as well. Phosphorylation of GIIβ alters the protein conformation such that GIIβ is no longer bound to NR1 mRNA. Loss of interaction with GIIβ allows NR1 mRNA to become temporarily “naked”. Endoribonclease(s) present in the vicinity are now able to attack the NR1 mRNA, eventually leading to NR1 mRNA degradation.