In approximately 15 percent of instances where couples are unable to conceive, the reason behind their struggle is unknown. Could it be because of “bad” eggs?
A study on female mice that occurred at the University of California San Diego School of Medicine and in the Division of Biological Sciences at UC San Diego could help explain some cases of infertility.
Cook-Andersen said this was definitely at least partially responsible for the mice’s infertility. It’s important for genes to be “turned off” in order for cells to advance to the next stage of development.
Researchers have identified a protein in mice that must be present in eggs in order for those eggs to develop. The protein is called ZFP36L2, or L2 for short. Without it, the eggs appear normal, but they cannot be fertilized by sperm. Female mice who do not have L2 in their eggs ovulate and are in all other ways healthy, but they cannot produce offspring.
Humans also have the L2 protein, so this discovery offers a new place to seek answers about infertility. Heidi Cook-Andersen, assistant professor of reproductive medicine and biological sciences at UC San Diego and physician at the UC San Diego-affiliated Reproductive Partners Fertility Center-San Diego, works with couples struggling to conceive. She says it can be very frustrating for everyone. Fertility tests come back normal and there just seems to be no answer as to why. However, there are still many important elements about fertility that have yet to be discovered, and L2 is one of them.
L2 is important because it activates decay of mRNA in cells when they are no longer needed. It is also needed for normal blood cell development.
To determine what effect L2 has on eggs, Cook-Andersen and her team worked with female mice who were engineered to completely lack the L2 protein in their eggs. These mice were set up with fertile male mice and were studied for 6 months. In that time, they didn’t have a single pup. However, at the same time, female mice with eggs rich in L2 produced pups regularly.
But why? The team found that the L2 deficient eggs were unable to undergo a crucial transcription silencing process that occurs during the final stages of egg growth. The conversion of genes was supposed to “shut off,” but they didn’t.
L2 and mRNA decay evidently play key roles in global transcriptional silencing. In the future, the research team plans to study L2 in humans. Now, they’re using the mouse study to learn more about global transcriptional silencing and to identify additional factors required to make a good egg.