Intricate ribosome composition and translational reprogramming in epithelial-mesenchymal transition.

Epithelial-mesenchymal transition (EMT) involves profound changes in cell morphology, driven by transcriptional and epigenetic reprogramming. However, evidence suggests that translation and ribosome composition also play key roles in establishing pathophysiological phenotypes. Using genome-wide analyses, we reported significant rearrangement of the translational landscape and machinery during EMT.

, a Powerful Model for Studying rRNA Modifications and Their Effects on Translation Fidelity.

Ribosomal RNA is a major component of the ribosome. This RNA plays a crucial role in ribosome functioning by ensuring the formation of the peptide bond between amino acids and the accurate decoding of the genetic code. The rRNA carries many chemical modifications that participate in its maturation, the formation of the ribosome and its functioning.

RiboDoc: A Docker-based package for ribosome profiling analysis.

Ribosome profiling (RiboSeq) has emerged as a powerful technique for studying the genome-wide regulation of translation in various cells. Several steps in the biological protocol have been improved, but the bioinformatics part of RiboSeq suffers from a lack of standardization, preventing the straightforward and complete reproduction of published results. Too many published studies provide insufficient detail about the bioinformatics pipeline used.

Evidence for rRNA 2'-O-methylation plasticity: Control of intrinsic translational capabilities of human ribosomes.

Ribosomal RNAs (rRNAs) are main effectors of messenger RNA (mRNA) decoding, peptide-bond formation, and ribosome dynamics during translation. Ribose 2'-O-methylation (2'-O-Me) is the most abundant rRNA chemical modification, and displays a complex pattern in rRNA. 2'-O-Me was shown to be essential for accurate and efficient protein synthesis in eukaryotic cells.

Global translational impacts of the loss of the tRNA modification tA in yeast.

The universal tRNA modification tA is found at position 37 of nearly all tRNAs decoding ANN codons. The absence of tA leads to severe growth defects in baker's yeast, phenotypes similar to those caused by defects in mcmsU synthesis. Mutants in mcmsU can be suppressed by overexpression of tRNA, but we show tA phenotypes could not be suppressed by expressing any individual ANN decoding tRNA, and tA and mcmsU are not determinants for each other's formation.