Zmat3 Is a Key Splicing Regulator in the p53 Tumor Suppression Program

Authors

Kathryn T Bieging-Rolett
Alyssa M Kaiser
David W Morgens
Anthony M Boutelle
Jose A Seoane
Eric L Van Nostrand
Changyu Zhu
Shauna L Houlihan
Stephano S Mello
Brian A Yee
Jacob McClendon
Sarah E Pierce
Ian P Winters
Mengxiong Wang
Andrew J Connolly
Scott W Lowe
Christina Curtis
Gene W Yeo
Monte M Winslow
Michael C Bassik
Laura D Attardi

Publication Date

11-5-2020

Journal

Molecular Cell

DOI

10.1016/j.molcel.2020.10.022

PMID

33157015

PMCID

PMC7654708

PubMedCentral® Posted Date

11-5-2021

PubMedCentral® Full Text Version

Author MSS

Published Open-Access

yes

Keywords

Adenocarcinoma, Alternative Splicing, Animals, Cell Cycle Proteins, Exons, Gene Expression Profiling, Genes, Tumor Suppressor, Humans, Liver Neoplasms, Male, Mice, Mice, Inbred ICR, Mice, SCID, RNA Interference, RNA Splicing, RNA-Binding Proteins, Tumor Suppressor Protein p53

Abstract

Although TP53 is the most commonly mutated gene in human cancers, the p53-dependent transcriptional programs mediating tumor suppression remain incompletely understood. Here, to uncover critical components downstream of p53 in tumor suppression, we perform unbiased RNAi and CRISPR-Cas9-based genetic screens in vivo. These screens converge upon the p53-inducible gene Zmat3, encoding an RNA-binding protein, and we demonstrate that ZMAT3 is an important tumor suppressor downstream of p53 in mouse Kras

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