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Competitive Sperm Swim Faster and Poison Peers

These sperm also take a straight path unlike their zigzagging rivals.

It turns out there's a difference in competitiveness between sperm swimming towards an egg, and it's down to genetics and one protein: RAC1.

If you thought it was by sheer luck that sperm make it all the way to the egg to fertilize it, you have just been proven wrong by a team of researchers at the Max Planck Institute for Molecular Genetics (MPIMG) in Berlin, Germany. 

The researchers explained in a study, published in the journal PLOS Genetics on February 4, how a genetic factor called "t-haplotype" awards the success of reaching the egg first to sperm that contain it, and it happens 99 percent of the time. 

In a first, the researchers pointed out that sperm with the t-haplotype moved faster than their peers without it. It also turned out that these faster-moving sperm were swimming straight, compared with their zigzagging competitors. 

And it comes down to RAC1, a protein that transmits signals from the outside of the sperm cell to the inside by activating other proteins. It essentially helps to direct the sperm in the right direction.

Competitive Sperm Swim Faster and Poison Peers
In direct competition, t-sperm wins against their normal peers (+) in their race to the egg using genetics.                                                           Source: Alexandra Amaral/MPIFG

On top of having assistance with directions, the t-haplotype sperm manage to poison their "normal" counterparts. These sperm not only produce a poison to stop their competitors, but they also create an antidote so that they themselves are protected from it, as Bernhard Herrmann, Director at the MPIMG and of the Institute of Medical Genetics at Charité – Universitätsmedizin Berlin, explained.

"Imagine a marathon, in which all participants get poisoned drinking water, but some runners also take an antidote," Herrmann compares. 

The team carried out its research on mice, so as to better understand the reasons for infertility in human males. Through their study, the researchers discovered that male mice with two copies of the t-haplotype were sterile because they produced only sperm with the t-haplotype, turning them all immotile. These cells have higher RAC1 levels. 

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However, having too low RAC1 levels also leads to disadvantages, as the sperm aren't able to move quickly enough. So the researchers speculate that aberrant RAC1 activity may be the underlying reason for particular forms of male infertility.

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