Do Fathers Matter?: What Science Is Telling Us About the Parent We've Overlooked

Do Fathers Matter?: What Science Is Telling Us About the Parent We've Overlooked by Paul Raeburn Read Free Book Online

Book: Do Fathers Matter?: What Science Is Telling Us About the Parent We've Overlooked by Paul Raeburn Read Free Book Online
Authors: Paul Raeburn
that cab.
    He recently published a fascinating analysis of the history of the Y chromosome. It is, of course, essential for sexual reproduction. Males have one X chromosome and one Y; females have two Xs. Mothers pass one or the other of their Xs to each child; fathers pass an X, which makes the child a girl, or a Y, which makes it a boy. Page and his team showed that the Y chromosome, which is much smaller than the X when seen under a microscope, is only a fragmentary remnant of what it once was. At one point, the X and Y chromosomes had about eight hundred genes in common. The Y has now lost all but nineteen of those genes.
    Are males disappearing?
    Not quite: the genes have been disappearing, but males themselves are not withering away. Most of the gene loss occurred a long time ago, and the Y now seems to have stabilized. It’s a lucky thing for fathers and for us: new research on the Y chromosome leads us on a fascinating tale of male genetics, which is far more complicated and important than you might expect, despite the loss of all those genes.
    *   *   *
    Until recently, we thought we had a pretty good understanding of how conception worked. Fathers and mothers each contribute 23 chromosomes to a fertilized egg, giving it the full complement of 46. (They all occur in matched pairs except the X and Y.) The fertilized egg then begins to divide into many kinds of cells, and ultimately grows into a fetus sharing traits from both its mother and its father. It seems simple enough. But as scientists developed the tools to fertilize eggs in the laboratory and study the process in greater detail, they discovered a much more interesting story.
    In the late 1970s, M. Azim Surani was a young developmental biologist in Cambridge, England, in the laboratory of the physiologist Robert G. Edwards—better known as half of the team of Steptoe and Edwards, who developed in vitro fertilization, or IVF. Edwards and gynecologist Patrick C. Steptoe were responsible for the 1978 birth of the world’s first so-called test-tube baby, Louise Brown, an achievement that would later be recognized with a Nobel Prize. Surani found the lab an enormously exciting place to be. The research on IVF was moving quickly when Surani joined the team, and Edwards wanted Surani to get involved in it. But Surani had a different idea.
    He was interested in the phenomenon known as parthenogenesis, which gets its name from the Greek words for virgin birth. It’s a form of reproduction in which healthy offspring arise from only a mother’s genes or only a father’s genes—not from a mix of the two, as is the case in sexual reproduction. Scientists knew at the time that it could occur in some fish, reptiles, and other animals. But it was not known to occur in mammals, including humans or laboratory mice. Surani wanted to see if he could manipulate mice in the lab to force a virgin birth.
    In mice and humans, the sperm and the egg each contribute one set of chromosomes to a fertilized egg, which then has a pair of them. That’s what it needs to divide and diversify. Combining two sets of a mother’s genes in an egg would theoretically accomplish the same thing: it would give the egg the correct number of chromosomes. Everything that was then known about genetics suggested that such an egg, even though all its genes came from females, should develop normally.
    By the time he left the Edwards lab, Surani and his assistant Sheila C. Barton had developed the tools he would need to manipulate genes and eggs. He used those tools to “fertilize” a mouse egg by inserting a copy of genes from another female. It didn’t work. He tried the experiment repeatedly and failed each time. The eggs with only mothers’ genes developed into tiny, fragile fetuses, but none of them survived. Shortly after they were implanted into foster mouse mothers, they died, riddled with genetic defects. Some grew more slowly and were smaller than normal embryos; others had

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