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Male infertility affects more than 20 million men worldwide and is a contributing cause of about 50% of infertility in couples. Male infertility is often caused by defects in the tail of the sperm, the flagellum, whose function is for sperm to swim toward an egg.
In addition, it has been seen that men with severe infertility can experience multiple sperm malformations, including flagella that are shortened, irregular, coiled, or even absent, which prevents them from swimming.
In humans, some genetic mutations produce malformed sperm, including those that affect sheath covering the sperm; mitochondria, which feed sperm while they swim; and a small sac, the achromosal vesicle, which releases the enzymes that allow a successful sperm to break through the outer lining of the egg to fertilize it.
To understand more about the causes of male infertility, the team at
Na Li y Ling Sun, of Guangzhou Women’s and Children’s Medical Center (China), collected sperm samples from infertile men and identified an individual with multiple defects affecting his sperm flagella.
Through genetic analysis they found a mutation in a largely unknown sperm protein, FSIP2 (Fibrous sheath interacting protein 2), a component of the fibrous sheath. “The fibrous sheath it covers the tails of sperm found in humans, mice and other species in which fertilization occurs within the body of the animal, ”explains Li.
And he adds: «offers to the tails of the sperm flexibility and strength, which is necessary for sperm to swim in the dense, sticky environment of the human body before they meet the egg. Interestingly, animals whose sperm swim in water because fertilization occurs outside the body, such as fish, do not have the FSIP2 protein or, at best, a faulty version.
To study the function of FSIP2, this team of researchers generated two sets of mice: one in which they reproduced the FSIP2 mutation from the human patient and another in which the animals hyperproduced the FSIP2 protein.
In this way they discovered that mice with the FSIP2 mutation they become infertile; their semen contained fewer live sperm and more than 50% could not swim forward.
In contrast, mice that overproduced the FSIP2 protein remained fertile and, compared to normal animals, had more than 7 times more super-long sperm, which could swim faster and be better able to fertilize an egg.
To understand the reasons for these changes in the flagella of sperm, the researchers analyzed the composition of the sperm.
They found that sperm from mice with the mutation FSIP2 had lower amounts of the proteins that make up the sheath that surrounds the sperm, the mitochondrial energy generators and the acrosomal vesicle.
However, sperm from mice that were overproducing FSIP2 generated a greater amount of sperm tail proteins, particularly in the fibrous sheath, which could allow sperm to swim more easily through the body.
The findings, published in
«Development», offer a new avenue to develop treatments for infertility, either by finding drugs that restore sperm movement or even finding ways to correct the debilitating mutation that originated the problem.
