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Bistable switches control memory and plasticity in cellular differentiation.

Lei Wang¹, Brandon L Walker, Stephen Iannaccone

¹Division of Hematology-Oncology-Transplantation, Children's Memorial Research Center, Department of Pediatrics, Northwestern University Feinberg School of Medicine, Chicago, IL 60614, USA.

Proceedings of the National Academy of Sciences of the United States of America

|April 16, 2009

Summary

Mitogen-activated protein kinase (MAPK) inhibition in human stromal cells induces osteogenic differentiation, revealing a bistable switch mechanism controlling cell fate plasticity. This cellular memory can be reset, allowing cells to regain their original myogenic ability.

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Area of Science:

Cell Biology
Developmental Biology
Stem Cell Biology

Background:

Cellular differentiation is typically irreversible in higher organisms, making postnatal tissue plasticity a controversial topic.
Understanding the mechanisms governing cell fate decisions is crucial for regenerative medicine and developmental biology.

Purpose of the Study:

To investigate the role of mitogen-activated protein kinase (MAPK) signaling in regulating cell fate plasticity in human bone marrow stromal cells.
To elucidate the molecular mechanisms underlying inducible differentiation and cellular memory in specialized cell types.

Main Methods:

Utilized a human bone marrow stromal cell-derived myogenic subclone for experimental manipulation.
Inhibited MAPK signaling to observe effects on myogenic and osteogenic differentiation.
Performed clonal analysis to characterize the nature of the induced osteogenic response.
Investigated the role of intracellular factors and protein synthesis in cellular memory.

Main Results:

MAPK inhibition suppressed myogenic ability and induced osteogenic differentiation, converting cells into satellite cell-like precursors.
The osteogenic response exhibited ultrasensitivity and all-or-none behavior, indicative of a bistable switch mechanism with stochastic noise.
Cellular memory of osteogenic differentiation was observed, dependent on an intracellular factor, and could be erased by cell division or protein synthesis inhibition.
MAPK inhibition effects also showed memory, regulated by an upstream bistable switch, and erasing this memory restored myogenic potential.

Conclusions:

Cell fate decisions are governed by a network of bistable switches controlling lineage-specific differentiation factors.
A competitive balance between these factors determines the ultimate cell fate.
This study demonstrates the dynamic nature of cellular differentiation, explaining its inherent stability and plasticity.