@article{7f95ac4463694657b925e91130185cab,
title = "Deconstructing transcriptional heterogeneity in pluripotent stem cells",
abstract = "Pluripotent stem cells (PSCs) are capable of dynamic interconversion between distinct substates; however, the regulatory circuits specifying these states and enabling transitions between them are not well understood. Here we set out to characterize transcriptional heterogeneity in mouse PSCs by single-cell expression profiling under different chemical and genetic perturbations. Signalling factors and developmental regulators show highly variable expression, with expression states for some variable genes heritable through multiple cell divisions. Expression variability and population heterogeneity can be influenced by perturbation of signalling pathways and chromatin regulators. Notably, either removal of mature microRNAs or pharmacological blockage of signalling pathways drives PSCs into a low-noise ground state characterized by a reconfigured pluripotency network, enhanced self-renewal and a distinct chromatin state, an effect mediated by opposing microRNA families acting on the Myc/Lin28/let-7 axis. These data provide insight into the nature of transcriptional heterogeneity in PSCs.",
author = "Kumar, {Roshan M.} and Patrick Cahan and Shalek, {Alex K.} and Rahul Satija and Keyser, {Ajay Daley} and Hu Li and Jin Zhang and Keith Pardee and David Gennert and Trombetta, {John J.} and Ferrante, {Thomas C.} and Aviv Regev and Daley, {George Q.} and Collins, {James J.}",
note = "Funding Information: Acknowledgements We thank members of the Collins and Daley laboratories for discussions. J.J.C. is supported by NIH grant R24DK092760 and the HHMI. G.Q.D. is supported by grants from the NIH (R01GM107536, R24DK092760, P50HG005550) and is an affiliate member of the Broad Institute and an investigator of the Manton Center for Orphan Disease Research and the Howard Hughes Medical Institute. A.R. is supported by the Broad Institute, the Klarman Cell Observatory at the Broad Institute, an NIH CEGS (1P50HG006193-01), an NIH Pioneer Award (DP1OD003958-01) and the HHMI. R.M.K. is supported by the Wyss Institute. P.C. is supported by NIDDK (K01DK096013) and received support from NHLBI (T32HL066987 and T32HL007623) and the Manton Center for Orphan Disease Research. R.S. was supported by an NIH Postdoctoral Fellowship (1F32HD075541-01). H.L. is supported by the Mayo Clinic Center for Individualized Medicine. Sequencing was performed by the Broad Institute Genomics Platform. Flow cytometry was performed in the Hematologic Neoplasia Flow Cytometry Facility at the Dana-Farber Cancer Institute and the BCH IDDRC Stem Cell Core Facility at Boston Children{\textquoteright}s Hospital supported by NIH-P30-HD18655. Single-cell qPCR experiments were performed at the BCH IDDRC Molecular Genetics Core Facility at Children{\textquoteright}s Hospital Boston supported by NIH-P30-HD18655. Fludigm C1 experiments were performed at the Broad Institute and the Biopolymers Facility at Harvard Medical School. Publisher Copyright: {\textcopyright} 2014 Macmillan Publishers Limited. All rights reserved.",
year = "2014",
month = dec,
day = "4",
doi = "10.1038/nature13920",
language = "English (US)",
volume = "516",
pages = "56--61",
journal = "Nature",
issn = "0028-0836",
publisher = "Nature Publishing Group",
number = "729",
}