such as "Introduction", "Conclusion"..etc
October 15, 2002 — Philadelphia, PA – In the
search to understand the nature of stem cells, researchers at the
University of Pennsylvania School of Medicine have identified a
regulatory gene that is crucial in maintaining a stem cell's ability to
self-renew. According to their findings, the Foxd3 gene is a required
factor for pluripotency – the ability of stem cells to turn into
different types of tissue – in the mammalian embryo. Their research is
presented in the October 15th issue of the journal Genes and
"Stem cells represent a unique tissue type with great potential for
disease therapy, but if we are to use stem cells then we ought to know
the basis of their abilities," said Patricia Labosky, PhD, an Assistant
Professor in the Department of Cell and Developmental Biology. "Among
the stem cell regulatory genes, it appears that Foxd3 gene expression
keeps stem cells from quickly differentiating – that is, developing
into different types of tissue – holding back the process so that an
embryo will have enough stem cells to continue developing normally."
To study the function of the Foxd3 gene, Labosky and her colleagues
generated mice with an inactivating mutation in the gene, and then
analyzed those mice to determine the role of the Foxd3 protein.
Foxd3-deficient embryos do not survive very long. While part of
the yolk sac forms, the inner cell mass that contains all the cells
that make up the body of the developing embryos fails to expand enough
to produce the embryo and some of the supportive tissues. Without
Foxd3, the mouse embryos simply could not maintain enough stem cells to
survive a crucial point in their development.
"Our findings implicate Foxd3 as one of the few genes serving
as a 'master switch' of the developing embryo," said Labosky. "These
genes determine the fate of cells by turning on or off other genes in
response to signals in the embryo."
Foxd3 joins previously identified genes, such as Oct4, Fgf4,
and Sox2, which control the pluripotency of embryonic stem cells in the
early stages of embryogenesis. In their experiments, Labosky and her
colleagues found that these genes are still expressed despite the lack
of Foxd3. This suggests Foxd3 functions either downstream of Oct4, Fgf4
and Sox2, or along a parallel pathway.
The researchers determined that normal embryonic development can be
restored by adding non-mutant embryonic stem cells to the Foxd3-mutant
embryos, indicating that Foxd3 acts in the inner cell mass and its
derivatives. According to Labosky, Foxd3 is a key regulator of
mammalian stem cells, with a clear counterpart in humans. Foxd3 gene
expression is a diagnostic characteristic of human embryonic stem
cells, suggesting that the gene may function in a similar fashion in
mouse and human cells.
"If we are to take advantage of stem cells as a clinical
therapeutic, then it is absolutely vital to identify the key regulatory
genes such as Foxd3 that control the process of cell differentiation,"
said Labosky. "Once we understand how these genes function we are that
much closer to being able to mold stem cells to meet our needs."
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