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Embyronic stem cell differentiation

Reference	BBS/E/R/00001601
Principal Investigator / Supervisor	Dr Thomas Burdon
Co-Investigators / Co-Supervisors
Institution	The Roslin Institute
Department	The Roslin Institute Department
Funding type	Research
Value (£)	432,750
Status	Completed
Type	Institute Project
Start date	01/10/2006
End date	31/03/2011
Duration	54 months

Abstract

Appropriate control of cellular differentiation is critical for coordinating growth and patterning during embryonic development and is essential for maintaining the health and reproductive fitness of adult organisms. Differences in the onset and extent of cellular differentiation underlie much of what is manifest as phenotypic variation in natural populations. However, when the processes are severely deregulated or disrupted they can lead to disease and compromise viability. Cellular differentiation is therefore an area of fundamental importance in biological research and improved understanding of the underlying processes has many beneficial applications in biotechnology, agriculture and biomedicine. All differentiated cells in a mammalian embryo originate from a cluster of unspecialised cells within the inner cell mass of the blastocyst. When these founder cells are explanted in culture they can give rise to pluriptotent embryonic stem (ES) cell lines that will proliferate indefinitely and retain the capacity to differentiate into all embryonic cell types. At present, ES cell lines are routinely derived from blastocysts of mice and a limited number of primates, including human, and represent a unique resource for investigating the basic molecular mechanisms that control differentiation. The ability of ES cells to differentiate into germ cells and reprogramme efficiently upon nuclear transfer also makes them an important tools for genetic modification. Efficient proliferation of undifferentiated ES cells in vitro requires continual suppression of differentiation by extrinsic factors. Disruption of prodifferentiative signaling pathways by mutation or pharmacological inhibition enhances ES cell self-renewal and reduces dependence on extrinsic factors. It seems therefore that tight regulation of prodifferentiative signals is critical for maintaining ES cell pluripotency and self-renewal, as well as driving acquisition of the differentiated phenotype.

Summary

unavailable

Committee	Closed Committee - Genes & Developmental Biology (GDB)
Research Topics	Stem Cells
Research Priority	X – Research Priority information not available
Research Initiative	X - not in an Initiative
Funding Scheme	X – not Funded via a specific Funding Scheme

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