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mRNA localization as a rheostat to regulate subcellular gene expression

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It is currently believed that certain messenger RNAs (mRNAs) are localized to distinct subcellular regions to efficiently target their encoded proteins. However, this simplistic model does not explain why in certain scenarios mRNA localization is dispensable for proper protein distribution. In other cases, mRNA localization is accompanied by translational silencing and degradation by the localization machinery. Here we propose that in certain scenarios mRNAs are localized so that they can either be stabilized and translated, or silenced and degraded, in response to the needs of the subcellular locale. In these cases, the localized mRNA, and its cadre of associated factors, act as a rheostat that regulates protein production and/or mRNA stability in response to the needs of its immediate subcellular environment. WIREs RNA 2017, 8:e1416. doi: 10.1002/wrna.1416 This article is categorized under: Translation > Translation Regulation RNA Export and Localization > RNA Localization RNA Turnover and Surveillance > Turnover/Surveillance Mechanisms
Localized translation as a means to regulate long‐term potentiation. Messenger ribonuclear protein (mRNP) complexes travel along the dendrite in a translationally silenced state. Upon synaptic excitation, these mRNPs are recruited, and become anchored to the base of the activated PSD, and are translated into proteins. Importantly, activated mRNAs are relatively static and do not diffuse to nearby PSDs. Translation of some PSD‐recruited mRNAs activates their destruction by NMD (see Box ), further restricting protein expression. The restricted expression of proteins stabilize the activated PSD while preventing the stabilization of nearby nonstimulated PSDs. This differential regulation of mRNA translation forms the basis of long‐term potentiation (LTP).
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Local regulation of CLB2 mRNA translation in the bud of S. cerevisiae. CLB2 mRNA is transported to the bud along actin cables by the She machinery. Its translation in the bud is likely responsive to bud‐specific conditions, and controls mitotic entry. Then CLB2 is degraded in TAM bodies and this regulates mitotic exit.
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Puf3p acts as a local or a global regulator of mitochondrial‐associated nuclear encoded mRNA. Puf3p translationally represses mRNAs coding for mitochondrial proteins at the surface of the mitochondria. Reduction of intracellular glucose level induces the phosphorylation of Puf3p, allowing the translation of Puf3p‐associated mRNA. It is unclear if these mRNAs are released and translated in the vicinity of mitochondria or if they become associated with mitochondrial‐tethered ribosomes. In contrast to this global regulation, local mitochondrial stress, such as ROS‐mediated damage, relieves Puf3p‐dependent repression of mRNAs allowing translation in the vicinity or on the surface of the mitochondrion thereby promoting mitochondrial repair and biogenesis. Severe or prolonged local mitochondrial stress induces Puf3p to sequester and repress mRNAs, which ultimately targets the destruction of the mitochondrion by mitophagy.
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RNA Turnover and Surveillance > Turnover/Surveillance Mechanisms
RNA Export and Localization > RNA Localization
Translation > Translation Regulation

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