Quantitative analysis by next generation sequencing of hematopoietic stem and progenitor cells (LSK) and of splenic B cells transcriptomes from wild-type and Usp3-knockout mice

Cesare Lancini; Gaetano Gargiulo; Paul C M van den Berk; Elisabetta Citterio

doi:10.1016/j.dib.2015.12.049

Quantitative analysis by next generation sequencing of hematopoietic stem and progenitor cells (LSK) and of splenic B cells transcriptomes from wild-type and Usp3-knockout mice

Data Brief. 2016 Jan 8:6:556-61. doi: 10.1016/j.dib.2015.12.049. eCollection 2016 Mar.

Authors

Cesare Lancini¹, Gaetano Gargiulo¹, Paul C M van den Berk², Elisabetta Citterio¹

Affiliations

¹ Division of Molecular Genetics, The Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX Amsterdam, The Netherlands.
² Division of Biological Stress Response, The Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX Amsterdam, The Netherlands.

Abstract

The data described here provide genome-wide expression profiles of murine primitive hematopoietic stem and progenitor cells (LSK) and of B cell populations, obtained by high throughput sequencing. Cells are derived from wild-type mice and from mice deficient for the ubiquitin-specific protease 3 (USP3; Usp3Δ/Δ). Modification of histone proteins by ubiquitin plays a crucial role in the cellular response to DNA damage (DDR) (Jackson and Durocher, 2013) [1]. USP3 is a histone H2A deubiquitinating enzyme (DUB) that regulates ubiquitin-dependent DDR in response to DNA double-strand breaks (Nicassio et al., 2007; Doil et al., 2008) [2], [3]. Deletion of USP3 in mice increases the incidence of spontaneous tumors and affects hematopoiesis [4]. In particular, Usp3-knockout mice show progressive loss of B and T cells and decreased functional potential of hematopoietic stem cells (HSCs) during aging. USP3-deficient cells, including HSCs, display enhanced histone ubiquitination, accumulate spontaneous DNA damage and are hypersensitive to ionizing radiation (Lancini et al., 2014) [4]. To address whether USP3 loss leads to deregulation of specific molecular pathways relevant to HSC homeostasis and/or B cell development, we have employed the RNA-sequencing technology and investigated transcriptional differences between wild-type and Usp3Δ/Δ LSK, naïve B cells or in vitro activated B cells. The data relate to the research article "Tight regulation of ubiquitin-mediated DNA damage response by USP3 preserves the functional integrity of hematopoietic stem cells" (Lancini et al., 2014) [4]. The RNA-sequencing and analysis data sets have been deposited in NCBI׳s Gene Expression Omnibus (Edgar et al., 2002) [5] and are accessible through GEO Series accession number GSE58495 (http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE58495). With this article, we present validation of the RNA-seq data set through quantitative real-time PCR and comparative analysis.

Keywords: B cell; BM, bone marrow; DDR, DNA damage response; DNA damage response (DDR); DNA double-strand breaks (DSBs); DUBs, deubiquitinating enzymes; Deubiquitinating enzymes (DUBs); HSC, hematopoietic stem cell; Hematopoietic stem and progenitor cells (HSPC); Hematopoietic stem cells (HSC); Histone H2A; LSK; LSK, Lin-Sca1+ cKit+ cells; RNA-seq; RNA-seq, RNA sequencing; Transcriptional profiling; USP3, Ub-specific protease 3; Ub, ubiquitin; Ubiquitin; Ubiquitin-specific protease 3 (USP3).