Dynein proteins give fly sperm a competitive edge

Sperm from 2 males (red and green) competing inside a female fruit fly. Image by Scott Pitnick via futurity.org

Every species has some genes that never existed before in evolutionary history, but where do new genes come from? Many new genes are made by copy-and-paste: old genes get copied, rearranged and pasted together with parts of other genes, plus some good ol’ junk DNA. The result: a piece of DNA that usually gets tossed out as an experiment gone bad. But sometimes, those new genes give their owners a competitive edge and they become part of the genome of an entire species.

More often than you might expect, new genes become male-specific and play important roles in male fertility. These genes get fast-tracked, becoming quickly “fixed” in the population because of the advantage they give to the boys in that age-old competition: who can make the most babies. New research into a group of newly evolved sperm genes in Drosophila melanogaster shows just how quickly new genes can become indispensable. The research was published last week in Proceedings of the National Academy of Sciences (see link at bottom).

Evolution is usually a frustratingly slow process, but sex has a way of speeding it up. The “goal” of any gene is to get made into as many copies as possible. A gene that helps its owner get a little bit more food than its neighbor may or may not actually lead to more babies, so it’s not going to spread all that fast. On the other hand, if a gene has a direct effect on how many offspring get made, it can spread very quickly. And what could be more direct than boosting the competitive ability of sperm?

In the fruit fly Drosophila melanogaster, a group of at least 4 male-specific genes have rapidly evolved together in the last 5.4 million years. The genes are called Sperm dynein intermediate chain (Sdic) 1 through 4. Dyneins are motor proteins that can move things around inside cells or that help to move cell flagella (like the tail of a sperm). The Sdic genes are located next to each other on the X chromosome. They evolved from a mixture of two other genes, plus some “junk” DNA, creating the first Sdic gene about 5.4 million years ago. After that, they quickly spread through the fruit fly population. After the first Sdic gene was formed, the copy-and-paste events that created the other 3 happened within the last 102-180 thousand years ago and also spread super-quickly. This is pretty much the blink of an eye in evolution terms. The authors of the study wanted to know why these genes were important enough to get fast-tracked through evolution.

Biologists have a tried-and-true method for figuring out why genes are important: break them and see what goes wrong. The authors deleted all of the Sdic genes (not an easy feat!) and tested these mutant males’ fertility. At first, they saw no defects: the males had normal testes and their sperm seemed happy enough.

Photo credit: T. Chapman in PLoS Biology; Vol. 6, No. 7, e179; July 29, 2008.

Next, they looked at whether the sperm could actually fertilize eggs normally. All of the males with Sdic deletions (mutant males) could fertilize eggs. Even more surprising: there was no difference in the number of offspring from mutant males vs. normal males.

So, why are the Sdic genes so important? The first set of experiments only looked at the number of offspring when one male mates to one female. But in nature, female fruit flies will mate with more than one male, so the ability to outcompete other males is extremely important.

To find if Sdic genes are involved in sperm competition, the authors pitted mutant males against normal males. They first mated a female to a standard male. Three days later they mated the same female either to a mutant male or a normal (control) male and counted how many of the offspring were from each male. This is easy in flies, because you just have to look at the eye color of the offspring.

This experiment measures the ability of the second male’s sperm to displace sperm from the first male. Normally, the second male has a huge advantage and sires most of the offspring. But even a small defect in the ability to knock the first male’s sperm out of storage could have dire consequences for the second male.

The bottom line: mutant sperm were worse at displacing the first male’s sperm.

The result was consistent between experiments, but not huge. The second male still always has the advantage. But, mutant sperm performed worse than normal sperm by a few percentage points. Also keep in mind that this was a controlled experiment in the lab. Males were only mated when at their peak fertility. Females only had to mate with 2 males. In the wild, females will mate with many males, and some males may have less sperm available at mating because they’ve also mated many times. So, finding even a small difference in the lab suggests these genes are very important for fertility in the wild.

Altogether, these results show that the Sdic genes are important for fertility. Natural selection drove the evolution of these genes because they gave males a competitive edge. These results are important because they clearly demonstrate that male-male competition can drive new genes to become very quickly integrated into existing pathways like sperm development. In other words, sex leads to new genes.


Yeh, S., Do, T., Chan, C., Cordova, A., Carranza, F., Yamamoto, E., Abbassi, M., Gandasetiawan, K., Librado, P., Damia, E., Dimitri, P., Rozas, J., Hartl, D., Roote, J., & Ranz, J. (2012). Functional evidence that a recently evolved Drosophila sperm-specific gene boosts sperm competition Proceedings of the National Academy of Sciences, 109 (6), 2043-2048 DOI: 10.1073/pnas.1121327109

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