Single cell RNA-seq and ATAC-seq analysis of cardiac progenitor cell transition states and lineage settlement
Guangshuai Jia,
Jens Preussner,
Xi Chen,
Stefan Guenther,
Xuejun Yuan,
Michail Yekelchyk,
Carsten Kuenne,
Mario Looso,
Yonggang Zhou,
Sarah Teichmann and
Thomas Braun ()
Additional contact information
Guangshuai Jia: Max Planck Institute for Heart and Lung Research
Jens Preussner: Max Planck Institute for Heart and Lung Research
Xi Chen: Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus
Stefan Guenther: Max Planck Institute for Heart and Lung Research
Xuejun Yuan: Max Planck Institute for Heart and Lung Research
Michail Yekelchyk: Max Planck Institute for Heart and Lung Research
Carsten Kuenne: Max Planck Institute for Heart and Lung Research
Mario Looso: Max Planck Institute for Heart and Lung Research
Yonggang Zhou: Max Planck Institute for Heart and Lung Research
Sarah Teichmann: Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus
Thomas Braun: Max Planck Institute for Heart and Lung Research
Nature Communications, 2018, vol. 9, issue 1, 1-17
Abstract:
Abstract Formation and segregation of cell lineages forming the heart have been studied extensively but the underlying gene regulatory networks and epigenetic changes driving cell fate transitions during early cardiogenesis are still only partially understood. Here, we comprehensively characterize mouse cardiac progenitor cells (CPCs) marked by Nkx2-5 and Isl1 expression from E7.5 to E9.5 using single-cell RNA sequencing and transposase-accessible chromatin profiling (ATAC-seq). By leveraging on cell-to-cell transcriptome and chromatin accessibility heterogeneity, we identify different previously unknown cardiac subpopulations. Reconstruction of developmental trajectories reveal that multipotent Isl1+ CPC pass through an attractor state before separating into different developmental branches, whereas extended expression of Nkx2-5 commits CPC to an unidirectional cardiomyocyte fate. Furthermore, we show that CPC fate transitions are associated with distinct open chromatin states critically depending on Isl1 and Nkx2-5. Our data provide a model of transcriptional and epigenetic regulations during cardiac progenitor cell fate decisions at single-cell resolution.
Date: 2018
References: Add references at CitEc
Citations: View citations in EconPapers (4)
Downloads: (external link)
https://www.nature.com/articles/s41467-018-07307-6 Abstract (text/html)
Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.
Export reference: BibTeX
RIS (EndNote, ProCite, RefMan)
HTML/Text
Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:9:y:2018:i:1:d:10.1038_s41467-018-07307-6
Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/
DOI: 10.1038/s41467-018-07307-6
Access Statistics for this article
Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie
More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().