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December 2008 — The mechanism whereby
embryonic cells stop being flexible and turn into more mature cells
that can develop into specific tissues has been discovered by
scientists at the Hebrew University of Jerusalem. The discovery has
significant consequences towards furthering research that will
eventually make possible medical cell replacement therapy based on the
use of embryonic cells.
At a very early stage of human development, all cells of the embryo
are identical, but unlike adult cells are very flexible and carry
within them the potential to become any tissue type, whether it be
muscle, skin, liver or brain.
This cell differentiation process begins at about the time that the
embryo settles into the uterus. In terms of the inner workings of the
cell, this involves two main control mechanisms. On the one hand, the
genes that keep the embryo in their fully potent state are turned off,
and at the same time, tissue-specific genes are turned on. By
activating a certain set of genes, the embryo can make muscle cells. By
turning on a different set, these same immature cells can become liver.
Other gene sets are responsible for additional tissues.
In a recent paper, published in the journal, Nature Structural and
Molecular Biology, Professors Yehudit Bergman and Howard Cedar of the
Hebrew University-Hadassah Medical School have deciphered the mechanism
whereby embryonic cells stop being flexible and turn into more mature
cells that can differentiate into specific tissues. Bergman is the
Morley Goldblatt Professor of Cancer Research and Experimental Medicine
and Cedar is the Harry and Helen L. Brenner Professor of Molecular
Biology at the Medical School.
They found in their experiments, using embryos from laboratory mice
and cells that grow in culture, that this entire process is actually
controlled by a single gene, called G9a, which itself is capable of
directing a whole program of changes that involves turning off a large
set of genes so that they remain locked for the entire lifetime of the
organism, thereby unable to activate any further cell flexibility.
Their studies shed light not only on this central process, but also
can have consequences for medical treatment. One of the biggest
challenges today is to generate new tissues for replacing damaged cells
in a variety of different diseases, such as Parkinson’s disease or
diabetes. Many efforts have been aimed at “reprogramming”
readily-available adult cells, but scientists have discovered that it
is almost impossible to do this, mainly because normal tissues are
locked in their fixed program and have lost their ability to convert
back to fully potent, flexible, embryonic cells.
Now, with the new information discovered by Bergman and Cedar, the
molecular program that is responsible for turning off cell flexibility
has been identified, and this may clear the way towards developing new
approaches to program cells in a controlled and specific manner.
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