Abstract
First identified 20 years ago as an RNA polymerase II-associated putative histone acetyltransferase, the conserved Elongator complex has since been recognized as the central player of a complex, regulated, and biologically relevant epitranscriptomic pathway targeting the wobble uridine of some tRNAs. Numerous studies have contributed to three emerging concepts resulting from anticodon modification by Elongator: the codon-specific control of translation, the ability of reprogramming translation in various physiological or pathological contexts, and the maintenance of proteome integrity by counteracting protein aggregation. These three aspects of tRNA modification by Elongator constitute a new layer of regulation that fundamentally contributes to gene expression and are now recognized as being critically involved in various human diseases.
Highlights
As a model organism, yeast has contributed enormously to most, if not all, aspects of our understanding of the fundamental biology of eukaryotes, ranging from cell cycle, cytoskeleton, autophagy, chromosome biology, metabolism, and gene expression
The Saccharomyces cerevisiae (S. cerevisiae, budding yeast) Elongator complex was found to be associated with the CTD
(C-terminal domain) hyperphosphorylated form of RNA polymerase II (Pol II), which was already known by that time to represent the elongating version of the Pol II complex [1]
Summary
Yeast has contributed enormously to most, if not all, aspects of our understanding of the fundamental biology of eukaryotes, ranging from cell cycle, cytoskeleton, autophagy, chromosome biology, metabolism, and gene expression. Further works functionally connected mRNAs may result from their skewed codon content and dependency on a have these original findings, whenthe it was shown that the translation of present an increasing list givensupported tRNA modification pathway, namely elongator/Trm pathway in the case [39]. The basis for the requirement of the Elongator-dependent tRNA modification has long been suspected to result from the low-stacking capacity of the unmodified AAA, GAA, and CAA codons, and the necessity to offset their translational inefficiency This possibility was formally proven by the team of Sebastian Leidel in 2015 using ribosome profiling. The activity of Elongator could be modulated, as seen for example in the case of the reciprocal regulation of the TOR pathway and Elongator [44], but maintained at a level avoiding global proteome-scale proteotoxic stress
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