Abstract
Upsetting the Dogma: Germline Selection in Human Males
Highlights
As early as 1912, Wilhelm Weinberg, the visionary human geneticist, noted that infants with achondroplasia tended to be born late in their sibship [1]
An attractive idea for the nature of the selection is that among the asymmetrical spermatogonial divisions, producing one daughter cell like the parent and one that develops into a sperm cell, occasional symmetrical divisions occur (Figure 1)
These, confer a large selective advantage by producing twice as many cell descendants. Arnheim and his colleagues attacked the problem head-on, studying the mutation underlying Apert syndrome [4] and, in this issue of PLoS Genetics, the mutation involved in multiple endocrine neoplasia type 2B (MEN2B) [5]
Summary
As early as 1912, Wilhelm Weinberg, the visionary human geneticist, noted that infants with achondroplasia (short-limbed dwarfism) tended to be born late in their sibship [1]. There was a large increase in mutations with paternal age. They studied FGFR2, which mutates to cause Apert syndrome. Using an enzyme that cuts the normal but not the mutant DNA at the relevant site, they identified FGFR2 mutations in sperm from normal males.
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