Gong et al. 2021 (PRJNA605444)

General Details

Title Male-specific lymphomagenesis by serial inverse dysregulation of the RNA helicases DDX3X and DDX3Y.
Organism
Number of Samples 20
Release Date 2020/01/09 00:00
Sequencing Types
Protocol Details

Study Links

Repository Details

SRA SRP247659
ENA SRP247659
GEO GSE143393
BioProject PRJNA605444

Publication

Title
Authors Gong C,Krupka JA,Gao J,Grigoropoulos NF,Giotopoulos G,Asby R,Screen M,Usheva Z,Cucco F,Barrans S,Painter D,Zaini NBM,Haupl B,Bornelöv S,Ruiz De Los Mozos I,Meng W,Zhou P,Blain AE,Forde S,Matthews J,Khim Tan MG,Burke GAA,Sze SK,Beer P,Burton C,Campbell P,Rand V,Turner SD,Ule J,Roman E,Tooze R,Oellerich T,Huntly BJ,Turner M,Du MQ,Samarajiwa SA,Hodson DJ
Journal Molecular cell
Publication Date 2021 Oct 7
Abstract DDX3X is a ubiquitously expressed RNA helicase involved in multiple stages of RNA biogenesis. DDX3X is frequently mutated in Burkitt lymphoma, but the functional basis for this is unknown. Here, we show that loss-of-function DDX3X mutations are also enriched in MYC-translocated diffuse large B cell lymphoma and reveal functional cooperation between mutant DDX3X and MYC. DDX3X promotes the translation of mRNA encoding components of the core translational machinery, thereby driving global protein synthesis. Loss-of-function DDX3X mutations moderate MYC-driven global protein synthesis, thereby buffering MYC-induced proteotoxic stress during early lymphomagenesis. Established lymphoma cells restore full protein synthetic capacity by aberrant expression of DDX3Y, a Y chromosome homolog, the expression of which is normally restricted to the testis. These findings show that DDX3X loss of function can buffer MYC-driven proteotoxic stress and highlight the capacity of male B cell lymphomas to then compensate for this loss by ectopic DDX3Y expression. Copyright © 2021 The Author(s). Published by Elsevier Inc. All rights reserved.
PMC
PMID 34437837
DOI
Run Accession Study Accession Scientific Name Cell Line Library Type Treatment GWIPS-viz Trips-Viz Reads BAM BigWig (F) BigWig (R)
SRR11041329 PRJNA605444 Homo sapiens U2OS Ribo-Seq
SRR11041330 PRJNA605444 Homo sapiens U2OS Ribo-Seq
SRR11041300 PRJNA605444 Homo sapiens Mutu Ribo-Seq
SRR11041301 PRJNA605444 Homo sapiens Mutu Ribo-Seq
SRR11041302 PRJNA605444 Homo sapiens Mutu Ribo-Seq
SRR11041303 PRJNA605444 Homo sapiens Mutu Ribo-Seq
SRR11041304 PRJNA605444 Homo sapiens Mutu Ribo-Seq
SRR11041305 PRJNA605444 Homo sapiens Mutu Ribo-Seq
SRR11041306 PRJNA605444 Homo sapiens Mutu Ribo-Seq
SRR11041307 PRJNA605444 Homo sapiens Mutu Ribo-Seq
SRR11041319 PRJNA605444 Homo sapiens U2OS Ribo-Seq
SRR11041320 PRJNA605444 Homo sapiens U2OS Ribo-Seq
SRR11041321 PRJNA605444 Homo sapiens U2OS Ribo-Seq
SRR11041322 PRJNA605444 Homo sapiens U2OS Ribo-Seq
SRR11041323 PRJNA605444 Homo sapiens U2OS Ribo-Seq
SRR11041324 PRJNA605444 Homo sapiens U2OS Ribo-Seq
SRR11041325 PRJNA605444 Homo sapiens U2OS Ribo-Seq
SRR11041326 PRJNA605444 Homo sapiens U2OS Ribo-Seq
SRR11041327 PRJNA605444 Homo sapiens U2OS Ribo-Seq
SRR11041328 PRJNA605444 Homo sapiens U2OS Ribo-Seq
Run Accession Study Accession Scientific Name Cell Line Library Type Treatment GWIPS-viz Trips-Viz Reads BAM BigWig (F) BigWig (R)

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