In competitive swimming, athletes will slim down and shave themselves to get a speed boost. Scientists have discovered sperm do the same thing, using a molecule that forces the cell to super-compact itself for a swimming advantage.
Genetic material is passed on through sperm via long strains of DNA. But one disadvantage of these strands is their giant size when unwound. As a response to this disadvantage, the body has developed a method for packing DNA strands up for easy transport. The DNA is bound up around molecules called histones and made into a dense genetic material called chromatin. This winding process is achieved by proteins grabbing onto tags distributed throughout the chromatin.
Of course, as compact as this material is, these little sperm cells try to get every advantage they can. That's where this newly discovered protein, Brdt, comes in. After the histones bind with this special protein, the sperm cell goes through a process of hypercompaction. When this protein is absent, the hypercompaction doesn't take place. The scientists, from the European Molecular Biology Laboratory, aren't sure if this is because of the special nature of Brdt or because Brdt is merely the last protein in the histone-binding sequence.
Scientists hope to use this new information about sperm development, released this week in Nature magazine, to find the link between hypercompaction and infertility. But it makes sense: if this extra phase of compaction transforms sperm from the fat kids at the pool who always belly-flop off the diving board into little Michael Phelpses, it's pretty clear why mice lacking this Brdt protein are infertile.
Putting the squeeze on sperm DNA [PhysOrg]
(Image: an X-ray crystallography image of the Brdt tags (the cyan strands) settled into the Brdt binding site. Also visible are two less-compact chromatin clumps, top left in blue, and two hypercompact versions, bottom right. Image from EMBL/IBS.)