By Sofie Bates
Females are born with a finite number of eggs that are steadily depleted throughout their lifetime. This reserve of eggs is selected from a much larger pool of millions of precursor cells, or oocytes, that form during fetal life. So there is a substantial amount of quality control during the process of forming an egg cell, or ovum, that weeds out all but the highest quality cells. New research from Neil Hunter’s laboratory at UC Davis reveals the surprising way that this critical oocyte quality control process works.
Homologous Recombination Can Cause More Breaks As It Fixes Them
The traditional view of cancer is that a cell has to sustain a series of hits to its DNA before its defenses break down enough for it to turn cancerous. But cancer researchers have also found that cells can experience very rapid and widespread DNA damage that could quickly lead to cancer or developmental defects.
Now researchers at the University of California, Davis, have found that these complex chromosomal rearrangements can be triggered in a single event when a process used to repair DNA breaks, homologous recombination, goes wrong. The work is published Aug. 10 in the journal Cell.
Where would we be without meiosis and recombination? For a start, none of us sexually reproducing organisms would be here, because that’s how sperm and eggs are made. And when meiosis doesn’t work properly, it can lead to infertility, miscarriage, birth defects and developmental disorders.
Neil Hunter’s laboratory at the UC Davis College of Biological Sciences is teasing out the complex details of how meiosis works. In a new paper published online Jan. 6 in the journal Science, Hunter’s group describes new key players in meiosis, proteins called SUMO and ubiquitin and molecular machines called proteasomes. Ubiquitin is already well-known as a small protein that “tags” other proteins to be destroyed by proteasomes (wood chippers for proteins). SUMO is a close relative of ubiquitin.
Full post: New Steps in the Meiosis Chromosome Dance
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