Pluripotency is increasingly recognized as a spectrum of cellstates defined by their growth conditions.
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Future studies should reveal the molecular basis for the differences in activities between the different cellstates.
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Such large distributions complicate the statistical evaluation of pharmacological treatments and the comparison of different cellstates.
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Our work highlights the superior power of proteome profiles to study protein complexes and their variants across cellstates.
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Second, we define quantitative measures of dynamical modularity, namely that global cellstates are discrete combinations of switch-level phenotypes.
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Single- cell transcriptomics has transformed our ability to characterize cellstates, but deep biological understanding requires more than a taxonomic listing of clusters.
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Modifications of DNA cytosine bases and histone posttranslational modifications play key roles in the control of gene expression and specification of cellstates.
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We demonstrate that compositional signatures of variable protein complexes have discriminative power beyond individual cellstates and can distinguish cancer cells from healthy ones.
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The need to derive and culture diverse cell or tissue types in vitro has prompted investigations on how changes in culture conditions affect cellstates.
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The complex interrelationships between pluripotency and chromatin factors are illustrated by X chromosome inactivation, regulatory control by noncoding RNAs, and environmental influences on cellstates.
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Ensembles with as many as 10,000 cells are used to simulate population synchronization and to compute transient number distributions from asynchronous initial cellstates.
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We sequenced 24,985 Hydra single- cell transcriptomes and identified the molecular signatures of a broad spectrum of cellstates, from stem cells to terminally differentiated cells.