The more precisely the position is determined, the less precisely the momentum is known in this instant, and vice versa (Werner Heisenberg, Uncertainty paper, 1927).
Chromatin remodeling and stem cell theory of relativity†
Version of Record online: 24 MAY 2004
Copyright © 2004 Wiley-Liss, Inc.
Journal of Cellular Physiology
Volume 201, Issue 1, pages 1–16, October 2004
How to Cite
Cerny, J. and Quesenberry, P. J. (2004), Chromatin remodeling and stem cell theory of relativity. J. Cell. Physiol., 201: 1–16. doi: 10.1002/jcp.20071
- Issue online: 21 JUL 2004
- Version of Record online: 24 MAY 2004
- Manuscript Accepted: 8 JAN 2004
- Manuscript Received: 4 JAN 2004
- NHLBI. Grant Number: R01 HL073749-01
- NIDDK. Grant Numbers: R01 DK60084-02, R01 DK27424-22
The field of stem cell biology is currently being redefined. Stem cell (hematopoietic and non-hematopoietic) differentiation has been considered hierarchical in nature, but recent data suggest that there is no progenitor/stem cell hierarchy, but rather a reversible continuum. The stem cell (hematopoietic and non-hematopoietic) phenotype, the total differentiation capacity (hematopoietic and non-hematopoietic), gene expression as well as other stem cell functional characteristics (homing, receptor and adhesion molecule expression) vary throughout a cell-cycle transit widely. This seems to be dependent on shifting chromatin and gene expression with cell-cycle transit. The published data on DNA methylation, histone acetylation, and also RNAi, the major regulators of gene expression, conjoins very well and provides an explanation for the major issues of stem cell biology. Those features of stem cells mentioned above can be rather difficult to apprehend when a classical hierarchy biology view is applied, but they become clear and easier to understand once they are correlated with the underlining epigenetic changes. We are entering a new era of stem cell biology the era of “chromatinomics.” We are one step closer to the practical use of cellular therapy for degenerative diseases. J. Cell. Physiol. 201: 1–16, 2004. © 2004 Wiley-Liss, Inc.