Cell type-specific novel long non-coding RNA and circular RNA in the BLUEPRINT hematopoietic transcriptomes atlas.
Martens, Joost HA
Stunnenberg, Hendrik G
MetadataShow full item record
Grassi, L., Izuogu, O. G., Jorge, N. A., Seyres, D., Bustamante, M., Burden, F., Farrow, S., et al. (2021). Cell type-specific novel long non-coding RNA and circular RNA in the BLUEPRINT hematopoietic transcriptomes atlas.. Haematologica, 106 (10), 2613-2623. https://doi.org/10.3324/haematol.2019.238147
Transcriptional profiling of hematopoietic cell subpopulations has helped characterize the developmental stages of the hematopoietic system and the molecular bases of malignant and non-malignant blood diseases for the past three decades. Previously, only the genes targeted by expression microarrays could be profiled genome wide. High-throughput RNA sequencing (RNA-seq), however, encompasses a broader repertoire of RNA molecules, without restriction to previously annotated genes. We analysed the BLUEPRINT consortium RNA- seq data for mature hematopoietic cell types. The data comprised 90 total RNA-seq samples, each composed of one of 27 cell types, and 32 small RNA-seq samples, each composed of one of 11 cell types. We estimated gene and isoform expression levels for each cell type using existing annotations from Ensembl. We then used guided transcriptome assembly to discover unannotated transcripts. We identified hundreds of novel non-coding RNA genes and showed that the majority have cell type dependent expression. We also characterized the expression of circular RNAs and found that these are also cell type specific. These analyses refine the active transcriptional landscape of mature hematopoietic cells, highlight abundant genes and transcriptional isoforms for each blood cell type, and provide a valuable resource for researchers of hematological development and diseases. Finally, we made the data accessible via a web-based interface: https://blueprint.haem.cam.ac.uk/bloodatlas/.
The authors would like to acknowledge the participation of National Institute of Health Research (NIHR) Cambridge BioResource volunteers and thank the NIHR Cambridge BioResource staff for their support. The work was funded by a grant from the European Commission 7th Framework Program (FP7/2007–2013, grant 282510, BLUEPRINT) to XE, PF, JHAM, MY, HGS and WHO. WHO is an NIHR senior investigator and receives funding from Bristol-Myers Squibb, the British Heart Foundation, the Medical Research Council and the NIHR. OGI, FJM, AF, JMM, LC and PF are funded by the Wellcome Trust (WT108749/Z/15/Z) with additional funding for specific project components such as GENCODE from the National Human Genome Research Institute of the National Institutes of Health (2U41HG007234), accordingly the content of this manuscript is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health. KD is a HSST trainee supported by NHS Health Education England. NF is funded by the NIHR Cambridge Biomedical Research Centre. FP is supported by the Fundação Carlos Chagas Filho de Amparo à Pesquisado Estado do Rio de Janeiro (FAPERJ; E-26/203.229/2016). NANJ is a recipient of a scholarship from the Coordenação de Aperfeiçoamento de Pessoal de Nível Superior - Brasil (CAPES; Finance Code 001). DS work has been supported in part by an Isaac Newton fellowship to MF. MF is supported by the British Heart Foundation (FS/18/53/33863).
Cambridge University Hospitals NHS Foundation Trust (CUH) (unknown)
Cambridge University Hospitals NHS Foundation Trust (CUH) (146281)
Embargo Lift Date
External DOI: https://doi.org/10.3324/haematol.2019.238147
This record's URL: https://www.repository.cam.ac.uk/handle/1810/307970
All rights reserved