Mari Mito

The paper introduces a method to quantify tRNA in low-input samples using RNA-dependent RNA amplification with T7 polymerase, showing reproducible and quantitative results.

The paper investigates mitochondrial translation termination, recycling, and quality control mechanisms using Ribo-Seq and Disome-Seq, revealing roles of release factors and rescue mechanisms.

The paper shows how mimiviruses create a subcellular environment to overcome codon-tRNA mismatch by localizing viral mRNAs and proteins at the periphery of a viral factory.

This study investigates the role of coilin in mice by generating coilin mutants, revealing its involvement in snRNA modifications and the formation of novel condensates in spermatids.

The paper develops a semi-automated Ribo-Seq and Disome-Seq platform to analyze translation status across many samples, identifying factors regulating translation and revealing links between stop codon readthrough and mitochondrial translation deficiency in COVID-19.

This study shows that eIF4G2 is essential for intestinal stem cell maintenance and differentiation by facilitating the translation of histone modifiers.

This study identifies EIF3D as a key regulator of primed pluripotency through selective translational control of signaling pathways and p53 regulators.

This study shows that eRF1 transiently binds to UUA sense codons, causing ribosome stalling and triggering quality control mechanisms in human cells.

The paper examines translation variation across yeast genetic backgrounds and identifies a post-transcriptional buffering signature that affects essential genes and low-transcribed genes.

The paper shows that translational regulation, particularly through 5' leader uORFs, enhances cell-type distinction in the Drosophila nervous system by preferentially translating neuronal proteins in neurons.

This study develops a high-resolution mitochondrial ribosome profiling technique to analyze translation dynamics and regulation in mammals.

This paper introduces methods to absolute quantify ribosome flux on transcripts, revealing ribosome allocation under stress, aging, and across cell types.

The paper shows that gravity and mechanical forces influence mitochondrial translation by affecting signaling pathways and malonylation of the translational machinery.

Thor-Ribo-Seq enables ribosome profiling on low-input samples using RNA-dependent RNA amplification to assess ribosome traversal with codon resolution.

The paper identifies a fungal mutation that allows survival on plants producing toxic rocaglates by altering eIF4A, a target of these compounds.

The paper investigates paraspeckle formation in naked mole-rats, finding that nNEAT1_2 recruits different RNA binding proteins compared to mice.

This study identifies SFSV NSs as a viral protein that suppresses the integrated stress response by binding to eIF2B and preventing eIF2(P) from inhibiting nucleotide exchange.

The paper shows that eIF4A1, not eIF4A2, facilitates LARP1-mediated translation repression during mTORC1 inhibition by preferentially binding TOP mRNAs.

The paper shows splicing modulators cause translational repression by inducing condensate-prone intron-derived proteins that inhibit mTORC1 and trigger proteotoxic stress.

The paper identifies genome-wide ribosome collision sites in humans and zebrafish, revealing their sequence motifs and functional roles in protein synthesis.

This study shows that switching Neat1 isoforms from Neat1_1 to Neat1_2 in mice leads to loss of Neat1_1, increased Neat1_2, and hyperformed paraspeckles without affecting mouse development or growth.

The paper investigates the roles of NEAT1 isoforms, finding that NEAT1_1 is dispensable for tissue homeostasis and cancer cell growth, while NEAT1_2 is critical for paraspeckle formation and function.

The paper introduces UPA-Seq, a method to predict functional lncRNAs by measuring their differential sensitivity to UV crosslinking, finding that lncRNAs with greater UV sensitivity associate more with PrLD-containing proteins.

The paper introduces tChIP-Seq, a method to analyze cell type-specific epigenetic modifications, identifying neuronal genes and unknown functions in cortical neurons.