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Biology subjects

Arnoldi, M.

Publications and source records attributed to Arnoldi, M..

2 recordsLinked to original sources

Selective profiling of translationally active tRNAs and their dynamics under stress

During translation, transfer RNAs (tRNAs) deliver specific amino acids to the ribosome in a coordinated manner with the sequence encoded by the mRNA. Despite their central role in protein synthesis, their precise contribution to the modulation of translation remains poorly understood, primarily due to lack of methods to characterise tRNA abundances and their modifications from actively translating ribosomes. Here we develop tRIBO-seq, a simple and robust nanopore-based method to selectively capture ribosome-associated native tRNA populations (ribo-tRNAs) from actively translating ribosomes, providing tRNA abundance, modification and fragmentation information from a single experiment. Using tRIBO-seq, we find that ribo-tRNAs, but often not total tRNAs, are significantly altered upon stress. Notably, we find that tRNAome alterations strongly vary depending on the stress type: while viral infection and leucine deprivation leads to changes in ribo-tRNA abundances, methionine starvation causes a dramatic loss of methyl-based tRNA modifications. By contrast, we find that arsenite exposure does not alter tRNA abundances nor modification patterns, but rather causes major fragmentation events in selected subsets of ribo-tRNAs. Altogether, tRIBO-seq offers a robust and reproducible approach to map the full tRNA landscape -capturing tRNA abundance, modification and fragmentation patterns-, across both total and actively translating tRNA populations, revealing the dynamics of the tRNAome with unprecedented resolution, in a single experiment.

molecular biology↗

CHD8 Suppression Impacts on Histone H3 Lysine 36 Trimethylation and Alters RNA Alternative Splicing.

Disruptive mutations in the chromodomain helicase DNA binding protein 8 (CHD8) have been recurrently associated with Autism Spectrum Disorders (ASD). In normal cellular physiology, CHD8 co-purifies with MLL1 and MOF transcriptional activation complex, with elongating RNAPII and directly binds to DNA promoters and enhancers regions, thus a regulatory role in transcriptional initiation and elongation could be postulated. Here we investigated how chromatin landscape reacts to CHD8 suppression by analyzing a panel of histone modifications in induced pluripotent stem cell-derived neural progenitors. We interrogated transcriptionally active and repressed regions, as well as active and poised enhancers. CHD8 suppression led to significant reduction (47.82%) in histone H3K36me3 peaks at gene bodies, particularly impacting on transcriptional elongation chromatin states. H3K36me3 reduction specifically affects highly expressed, CHD8-bound genes. Histone H3K36me3 reduction associated to CHD8-suppression does not functionally impact on global transcriptional levels, but correlated with altered alternative splicing patterns of [~] 2000 protein coding genes implicated in "RNA splicing", "mitotic cell cycle phase transition" and "mRNA processing", especially affecting alternative first exon and exon skipping events. In summary, our results point toward broad molecular consequences of CHD8 suppression, implicating altered histone deposition/maintenance and RNA processing regulation as important regulatory processes in ASD.

genetics↗