Early transient suppression of c-myb mRNA levels and induction of differentiation in Friend erythroleukemia cells by the [Ca2+]i-increasing agents cyclopiazonic acid and thapsigargin.

Schaefer, András; Magócsi, Mária; Stöcker, Ulrich; Kósa, Ferenc; Marquardt, Hans

doi:10.1016/s0021-9258(17)37037-0

Cited by 38 publications

(2 citation statements)

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“…16 in [Tsuchiya at al 2020]), which was not seen in the DMSO model. This may be due to a difference in Ca2+ influx [Papp et al 2012] which controls key cell-fate processes including fertilization, early embryogenesis [Whitaker 2006], and differentiation [Yen et al 1987; Schaefer et al 1994; Dolmetsch et al 1997; Launay at al. 1999].…”

Section: Discussionmentioning

confidence: 99%

“…The achievement of cell-fate determination after 18h for DMSO and after 24h for atRA (Figures3B,C) occurs in these two models in different ways, although they converge at the same final state at 48h.In particular, we observed early global genome perturbation in the response to atRA (at 0-4h: see Fig.16in [Tsuchiya at al 2020]), which was not seen in the DMSO model. This may be due to a difference in Ca2+ influx[Papp et al 2012] which controls key cell-fate processes including fertilization, early embryogenesis[Whitaker 2006], and differentiation[Yen et al 1987;Schaefer et al 1994;Dolmetsch et al 1997; Launay at al. 1999].…”

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confidence: 99%

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A Unified Genomic Mechanism of Cell-Fate Change

Tsuchiya

Giuliani

Zimatore

et al. 2021

Preprint

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The purpose of our studies is to elucidate the nature of massive control of whole genome expression with a particular emphasis on cell-fate change. Whole genome expression is coordinated by the emergence of a critical point (CP: a peculiar set of bi-phasic genes) through the genome-engine. In response to stimuli, the genome expression self-organizes three critical states, each exhibiting distinct collective behaviors with its center of mass acting as a local attractor, coexisting with whole genome attractor (GA). Genome-engine mechanism accounts for local attractors interaction in phase space. The CP acts as the organizing center of cell-fate change, and its activation makes local perturbation spread over the genome affecting GA. The activation of CP is in turn elicited by ‘hot-spots’, genes with elevated temporal variance, normally in charge to keep genome expression at pace with microenvironment fluctuations. When hot-spots oscillation exceeds a given threshold, the CP synchronizes with the GA driving genome expression state transition. The expression synchronization wave invading the entire genome depends on the power law fusion-bursting dynamics of silencing pericentromere-associated heterochromatin domains and the consequent folding-unfolding status of transcribing euchromatin domains. The proposed mechanism is a unified step toward a time-evolutional transition theory of biological regulation.

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