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Wobble tRNA modification dependent protein aggregates modification

ABSTRACT: We want to assess the features of proteins whose aggregation depends on defects in traslation by the loss of the mcm5s2 modification on the urifdine in position 34 of some tRNAs.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Epithelial Cell, Cell Culture

DISEASE(S): Breast Cancer

SUBMITTER: Dominique Baiwir

LAB HEAD: Pierre CLOSE

PROVIDER: PXD019590 | Pride | 2021-02-24

REPOSITORIES: Pride

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Wobble tRNA modification and hydrophilic amino acid patterns dictate protein fate.

Rapino Francesca F Zhou Zhaoli Z Roncero Sanchez Ana Maria AM Joiret Marc M Seca Christian C El Hachem Najla N Valenti Gianluca G Latini Sara S Shostak Kateryna K Geris Liesbet L Li Ping P Huang Gang G Mazzucchelli Gabriel G Baiwir Dominique D Desmet Christophe J CJ Chariot Alain A Georges Michel M Close Pierre P

Nature communications 20210415 1

Regulation of mRNA translation elongation impacts nascent protein synthesis and integrity and plays a critical role in disease establishment. Here, we investigate features linking regulation of codon-dependent translation elongation to protein expression and homeostasis. Using knockdown models of enzymes that catalyze the mcm5s2 wobble uridine tRNA modification (U34-enzymes), we show that gene codon content is necessary but not sufficient to predict protein fate. ...[more]

PMID: 33859181

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Protein aggregation mediates protein complex stoichiometry in aneuploid cells, part 1

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2014-05-29 | E-GEOD-57989 | biostudies-arrayexpress

Evollutionally dynamic L1 regulation in embryonic stem cells

Project description:Mobile elements are important evolutionary forces that challenge genomic integrity. Long interspersed element-1 (L1, also known as LINE-1) is the only autonomous transposon still active in the human genome. It displays an unusual pattern of evolution, with at any given time a single active L1 lineage amplifying to thousands of copies before getting replaced by a new lineage likely under pressure of host restriction factors, which act notably by silencing L1 expression during early embryogenesis. Here, we demonstrate that in human embryonic stem cells (hESC) KAP1, the master co-factor of KRAB-containing zinc finger proteins (KRAB-ZFP) previously implicated in the restriction of endogenous retroviruses, represses a discrete subset of L1 lineages predicted to have entered the ancestral genome between 26.8 and 7.6 million years ago. In the mouse, we documented a similar chronologically conditioned pattern, albeit with a much contracted time scale. We could further identify an L1-binding KRAB-ZFP, suggesting that this rapidly evolving protein family is more globally responsible for L1 recognition. KAP1 knockdown in hESC induced the expression of KAP1-bound L1 elements, but their younger, human-specific counterparts (L1Hs) were unaffected. Instead, they were stimulated by depleting DNA methyltransferases, consistent with recent evidence demonstrating that the PIWI-piRNA pathway regulates L1Hs in hESC. Altogether, these data indicate that the early embryonic control of L1 is an evolutionary dynamic process, and support a model whereby newly emerged lineages are first suppressed by DNA methylation-inducing small RNA-based mechanisms, before KAP1-recruiting protein repressors are selected. HA-tagged Gm6871 ChIP-seq in mES cells, RNA-seq in control and Gm6871 KD mES cells, KAP1 ChIP-seq in WT mES cells, RNA-seq in control and DNMTs KD hES cells.

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Protein aggregation mediates protein complex stoichiometry in aneuploid cells, part 4

2020-05-26 | PXD011877 | Pride

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Protein aggregation mediates protein complex stoichiometry in aneuploid cells, part 5

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Protein aggregation mediates protein complex stoichiometry in aneuploid cells, part 6

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Protein aggregation mediates protein complex stoichiometry in aneuploid cells, part 3

2020-05-26 | PXD011876 | Pride

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Enhancer Sequence Variants and Transcription Factor Deregulation Synergize to Construct Pathogenic Regulatory Circuits in B Cell Lymphoma (ChIP-Seq, FAIRE-Seq)

Project description:Most B cell lymphomas arise in the germinal center (GC), where humoral immune responses evolve from potentially oncogenic cycles of mutation, proliferation, and clonal selection. Although lymphoma gene expression diverges significantly from GC-B cells, underlying mechanisms that alter the activities of corresponding regulatory elements (REs) remain elusive. Here we define the complete pathogenic circuitry of human follicular lymphoma (FL), which activates or decommissions transcriptional circuits from normal GC-B cells and commandeers enhancers from other lineages. Moreover, independent sets of transcription factors, whose expression is deregulated in FL, target commandeered versus decommissioned REs. Our approach reveals two distinct subtypes of low-grade FL, whose pathogenic circuitries resemble GC-B or activated B cells. Remarkably, FL-altered enhancers also are enriched for sequence variants, including somatic mutations, which disrupt transcription factor binding and expression of circuit-linked genes. Thus, the pathogenic regulatory circuitry of FL reveals distinct genetic and epigenetic etiologies for GC-B transformation. Molecular profiling of follicular lymphoma, resting peripheral blood and tonsillar B cells using Formaldehyde-Assisted Isolation of Regulatory Elements (FAIRE) and chromatin immunoprecipitation (H3ac and H3K27ac).

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