Text/Chen Gen
A baby is developed from a fertilized egg, which means that an egg must be fertilized with one of the 250 million sperm. However, in recent years, there have been a large number of studies pointing to the fact that male reproductive health is being compromised, among them, Western and industrialized countries have reported significant declines in sperm concentrations.
The decline in semen quality in humans may be becoming a regional or even global problem. Correspondingly, the incidence of infertility remains high, and the male factor accounts for about half of the reasons. Microscopically, in the process of sperm movement, its tail (that is, the flagella) plays a crucial role: the flagella must beat in a very precise and coordinated way to push the sperm forward.
Against this backdrop, a recent study in the journal Science revealed the physiological key to ensuring that sperm flagella beat at the correct rhythm. Studies have shown that the key lies in a protein modification mechanism, and animal experiments provide direct evidence that without this particular protein modification, sperm cannot maintain straight line movement, but can only spin in place, ultimately leading to male infertility.

Among them, the core of the sperm flagella is composed of tubulin proteins, along with tens of thousands of micromolecular motors, known as dyneins, which are closely coordinated and rhythmically bend the microtubules, causing the flagella to beat and turn. Tubulin is widely present in a variety of cells and is involved in a variety of physiological activities. In different types of cells, they are added to different "molecular labels" by a series of different enzymes to perform different functions.
In cells with flagella (or cilia) like sperm, scientists have found that a special glycine tag is added to the tubulin, so this process is called glycylation.
In the study, to explore what role glycine tags on tubulins play in the function of flagella and cilia, the scientists constructed a special type of genetically defective mouse: They were simultaneously missing two key enzymes that prevented the cell's flagella (or cilia) from being glycineated. It was found that male mice that could not be glycineated had problems with infertility.
Using computer-aided analysis, the researchers observed that the sperm of these mice were able to assemble the flagella normally and swim, but the rhythm of the flagella became disordered. As a result, the sperm cannot move in a straight line normally, but instead circle along a circular path. This abnormal pattern of movement means that the sperm will have a hard time reaching the oocytes to start fertilizing.
The researchers say their work shows that tubulin glycosylation regulates the movement of mammalian flagella by regulating the movement of axon dynamin. Lack of glycosylation leads to sperm motility disorders and male infertility in mice. Considering that human sperm are more susceptible to insufficient sperm motility than mouse sperm, this means that disruption of tubulin glycosylation may be the basis for some form of male infertility in humans.