In this week's Nature, Decode Genetics researchers publish genome sequencing data showing that children of older fathers have a higher de novo mutation rate. "Most notably, the diversity in mutation rate of single nucleotide polymorphisms is dominated by the age of the father at conception of the child," the researchers write, and the effect translates to about two mutations for every additional year of the father's age. The results suggest that father's age could increase the risk of conditions such as schizophrenia and autism.
Elsewhere, a team led by researchers from the International Rice Research Institute in the Philippines reports on the characterization of a gene that can enhance rice yields in crops that typically require phosphorus fertilizer. Additional analysis shows that the gene, dubbed phosphorus-starvation tolerance 1, or PSTOL1, enhances early root growth, enabling plants to acquire more phosphorus and other nutrients. Introducing this gene into various rice varieties could, the team says, "considerably enhance productivity under low phosphorus conditions."
Also in Nature, University of Washington in Seattle researchers detail the discovery that mice with only a single functional copy of the SCN1A gene, which encodes the voltage-gated sodium channel Nav1.1, display autism-like behavior. The findings indicate that Dravet's syndrome, a childhood epilepsy disorder caused by dysfunction of this sodium channel, is associated with the autistic and cognitive symptoms observed in patients. The mutation that impairs Nav1.1 also negatively affects GABA neurotransmission in the brain, and when mice were treated with clonazepam, a known positive modulator of GABA receptors, the autistic behavior is eliminated, suggesting a "potential therapeutic strategy for cognitive deficit and autism-spectrum behaviors in Dravet's syndrome," the researchers write.
The phrasing of this snipet
The phrasing of this snipet as well as a Genome Web article yesterday by Andrea Anderson seem to be very misleading. They state that the "mutation RATE" is higher in "the children of older fathers." Are the genomes within the cells of these children mutating faster than the genomes of their peers begat by younger fathers? That is what the phrasing quoted above implies. However what I understand from the synopses to be described by Steffenson is that more spontaneous mutations have accumulated in a father's germ cells after four (e.g.) decades of life than two. This is hardly surprising but rather inevitable. So my younger sibling's paternal genes are less identical to my father's original genome sequence than mine. Unless my father's genome was transcendently perfect and all base changes deleterious rather than likely to be neutral, I don't see any consequences here graver than ordinary biology.