The approval of
a new treatment method by which three parents will be able to beget a
child is being discussed since a few years in Great Britain and will
possibly become a reality in two years. The method is supposed to help
in eliminating the mother's genetic defects already in the test tube.
The defect lies in so-called mitochondria, the "power houses" of cells.
To get rid of defective mitochondria the nucleus of one egg cell has to
be transferred to another egg cell bearing intact mitochondria.
Scientists at the Vetmeduni Vienna show for the first time that even a
few defective mitochondria dragged along in the transfer could cause
diseases.
The results were published in Cell Reports.
Mitochondria
are cell organelles located within animal and human cells. They produce
energy for the organism, possess their own genetic material --
mitochondrial DNA (mtDNA) -- and are transmitted exclusively by the
mother. Depending on their activity and tasks, different numbers of
mitochondria are present in a cell -- usually a few hundred to a
thousand per body cell.
Inherited mitochondrial
disorders or so-called mitochondropathies occur in about one of 10,000
humans throughout the world. Diseases such as diabetes, stroke, cardiac
defects, epilepsy, or muscle weakness may originate from mitochondrial
defects. Inherited mitochondrial disorders have been incurable so far.
Therefore, efforts are now being made to enable women with this disease
to bear healthy children by means of nuclear transfer.
Mitochondria multiply at different rates
ADVERTISEMENT
Jörg
Burgstaller, a scientist and member of Gottfried Brem's research group
at the Vetmeduni Vienna, has been working for several years on the
genetics of mitochondria. It was known before that different types of
mitochondria within a cell can proliferate at different rates. However,
it was not known whether this is a singular phenomenon or if these cases
occur more frequently.
Burgstaller investigated this in four
newly bred mouse models which carried different mixtures of mitochondria
whose DNA were related to each other to a differing extent. This meant
no health problem for the mice since all mtDNAs are were fully
functional.
The outcome was: the more distantly two types of
mitochondria within an egg cell were related, the more frequently a
growth advantage was noted in favor of one of the two types of
mitochondria. When two different mtDNAs were equally common in cells of
an organ at the time of birth, one type was completely lost after a
while. One mitochondria variant had thus achieved a growth advantage
compared to the other variant and superseded the latter. This effect was
almost non-existent in genetically very similar mitochondria within the
cells; the ratio between the two types of mitochondria was not altered
in that case.
The effect is of significance in reproduction medicine
Burgstaller's
results may have effects on the planned introduction of the so called
"Three-Parent Baby" in Great Britain. Experts take the cell nucleus of
one human egg cell whose mitochondria have a defect and place it in an
egg cell with "healthy" mitochondria. The baby resulting from this
procedure has three parents, namely the mother whose cell nucleus is
used, the mother whose mitochondria are involved, and the father whose
sperm inseminated the egg cell.
However, this method raises the
following problem: in every nuclear transfer, a small number of
defective mitochondria are transferred into the healthy egg cell. "So
far it was believed that this minimal 'contamination' is of no
consequence for the baby. However, our data show that the effect may
have dramatic consequences on the health of the offspring. If the
mitochondria of both mothers are genetically very different, it may have
the same effects seen in the mouse model," says Burgstaller who
developed the theory together with co-author Joanna Poulton, Professor
of Mitochondrial Genetics at the John Radcliffe Hospital in Oxford. "One
mitochondrial type may be able to assert itself against the other. If
the assertive one happens to carry the defective mtDNA, the benefit of
the therapy would be jeopardized."
The solution to the "Three-Parent Baby" problem
Burgstaller
and his colleagues suggest the following solution to the problem: the
mtDNA of both mothers, i.e. the donor of the nucleus and the donor of
the mitochondria, should be analyzed in advance and aligned to each
other. So called "matching haplotypes" could prevent the dangerous
effect. In the future the effect may even be utilized in a targeted
manner to suppress defective mtDNA.
The work was conducted in
cooperation with BIAT (Biomodels Austria) and the technology platform
Vetcore at Vetmeduni Vienna, Joanna Poulton from John Radcliffe Hospital
in Oxford, Jaroslav Piálek from the Czech Academy of Sciences, and Iain
Johnston and Nick Jones from the Imperial College (London).
Story Source:
http://www.sciencedaily.com
No comments:
Post a Comment