New Hope For Infertility

In July 2006, Prof Nayernia published a paper in Developmental Cell where he showed that he and colleagues had created sperm cells from mouse embryonic stem cells and used these to fertilise mice eggs, resulting in seven live births.

Now, he has published in Gamete Biology another breakthrough paper. A team of scientist lead by Professor Nayernia has isolated mesenchymal stem cells from the bone marrow of the male volunteers and coaxed into becoming germ cells (partially developed sperm cells called spermatagonial cells). The genetic markers showed that these mesenchymal cells had indeed developed into spermatagonial cells. While in most men, the spermatogonial cells develop into mature, functional sperm cells, this natural progression was never achieved in this experiment.


(Image courtesy: Mail On Sunday)

Earlier Prof Nayernia had shown that when spermatogonial cells were created similarly from mouse bone arrow and transplanted into mouse testes, they underwent early meiosis but did not develop any further.

Talking about his newly published research paper, Prof Nayernia, of Newcastle University, said : "We're very excited about this discovery, particularly as our earlier work in mice suggests that we could develop this work even further. Our next goal is to see if we can get the spermatagonial stem cells to progress to mature sperm in the laboratory and this should take around three to five years of experiments.”

The experiments open a whole new avenue for not only infertile males, but also for gay couples. What was done with the male blood cells, could be done with female bone marrow. Exciting times, lie ahead.

A word of caution before the media rings this in as male infertility solved.
Firstly, the cells in this case have not developed into mature sperm.

Secondly, the earlier experiments with the stem cell redirected sperms had resulted in mice that had severe problems - they were all infertile and had breathing or walking difficulties. They also were growth impaired, either abnormally large or or small. And all had reduced life expectancy - they died within three days to five months of being born (normal lifespan is two years for healthy mice). Prof Nayernia had acknowledged then the abnormalities were probably due to genetic defects that arose in the creation of the sperm.


Of course, the technique has already provoked an ethical storm (and it was just published on the 11th!) and could soon be banned by the Government over concerns about the safety of using artificial sperm. Critics say that the treatment breaches moral boundaries, mostly because it would effectively render males redundant!! The technique could be adapted to grow eggs in a lab (and thus helping infertile women), but this seems to the critics a way of children being born through entirely artificial means!

Precaution needs to be taken before the use of this technique - the scientist themselves claim that work needs to be done, the process is far from perfect. But to blanket ban it would hurt several hundreds of infertile men (natural or those who underwent chemotherapy)..

Heights! Mapping the "Toy" Gene

Domesticated dogs are amazing in their variety - pocket size Yorkshire terriers to Great Danes! Ever wonder what accounts for that disparity?

Wonder no more. This week's issue of Science sees a study published that gives us a clue to how a mutation in a single locus regulates size in these creatures.

A team of more than 20 scientists from eight institutions (United States and the U.K.) toured the dog show circuit and collected blood from 3,241 canines of all sizes and shapes. They found that the reduced growth mapped to a locus, near the IGF1 gene. In human IGF1 plays a role in the growth from birth till adolescence.

In all the "toy" dogs tested (distantly related and reproductively isolated), there were mutations in the region next to IGF1. This is intriguing to see a single change map to all the small breeds, indicating that the change probably maps to the time when dogs evolved from their wolf-like ancestors. The same "small dog marker" however, is not found in the modern wolves.

Why is this so fascinating? Mostly because the entire study pinpoints a single allele to be responsible for the phenotypic variation (small size) and the result was achieved without doing a single cross!!