Signalling in stem cells

Meeting on Signal Transduction Determining the Fate of Stem Cells
Lynn E Heasley, Bryon E Petersen

Author Affiliations

  • Lynn E Heasley, 1 Department of Renal Medicine, C‐281, University of Colorado Health Sciences Center, 4200 E. Ninth Avenue, Denver, Colorado, 80262, USA
  • Bryon E Petersen, 2 Department of Pathology, Immunology and Laboratory Medicine, College of Medicine, University of Florida, PO Box 100275, Gainesville, Florida, 32610‐0275, USA

The meeting “Signal Transduction Determining the Fate of Stem Cells” was held at Montana State University in Bozeman, Montana, between August 9 and 12, 2003. The meeting was sponsored by the American Society for Cell Biology and was organized by G.L. Johnson and N. Terada.

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Many scientific meetings have been organized to present research findings on stem‐cell sources, their pluripotent nature and potential therapeutic applications for treating disease. The theme of this meeting was the signalling pathways that control stem‐cell maintenance and differentiation. In his keynote address, A. Spiegel (Bethesda, MD, USA) emphasized the high therapeutic potential of stem cells, and also the need to understand more about their unique cell and molecular biology to harness their therapeutic application. Although embryonic, haematopoietic and hepatic stem cells from humans are the obvious therapeutics, stem‐cell research in various organisms from flies to humans was presented at this meeting.

Signalling of stem‐cell proliferation and survival

A common feature of stem cells, regardless of origin and type, is their ability to undergo self‐renewal. Cultured stem cells, especially embryonic stem (ES) cells, exhibit a high rate of proliferation and a short cell cycle time (10–12 hours). Studies by S. Dalton (Athens, GA, USA) showed that ES cells have a unique cell cycle that lacks complete G1 and G2 gap phases (Stead et al, 2002). The activity of cyclin‐dependent kinases (Cdks) is constitutively high relative to their activity in somatic cells such as mouse embryo fibroblasts. Genes that are the target of the E2F transcription factor are also constitutively active, consistent with the negligible activity of the retinoblastoma (Rb) protein pathway in these cells. Analysis of Cdk activity in mouse ES cells reveals a novel, constitutively active Cdk6–cyclin D3 complex that is rapidly downregulated following ES cell differentiation. Importantly, this Cdk–cyclin complex is insensitive to the defined Cdk inhibitors such as p16. …