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Published on: January 26, 2024
ADAM20 Participates Modestly to Fertilization as Its Absence Leads to In Vitro Hypofertility in Mouse
Marie-Sophie Girault1, Sophie Dupuis1, Rémi Pierre1
1Institut Cochin, INSERM, CNRS, Université Paris Cité, Paris, France.
Abstract:
A mutation of the ADAM20 gene was described in an infertile patient whose spermatozoa were observed accumulating in the perivitelline space of oocytes. To decipher its role in the fertilization process, we produced a mouse model knock-out (KO) for the Adam20 gene. Surprisingly, Adam20-KO males showed an in vivo fertility similar to their wild-type littermates and had normal sperm counts and morphology. However, they presented a reduced fertility in in vitro fertilization assays. To explore the hypothesis that the two flanking genes Adam25 and Adam39 could compensate the lack of Adam20 given their very high homology, we produced a triple KO deleting these three neighbor genes simultaneously. The phenotype was strictly identical to that of the single gene deletion. Therefore, ADAM20, ADAM25, and ADAM39 are not essential proteins for fertilization in mice but they seem to participate modestly to the process. Adam20-KO males are fertile in vivo but have a reduced fertility in vitro. Males deleted for three neighbor and very homologous genes (Adam20, Adam25, and Adam39) have the same phenotype as the simple Adam20-KO. These genes are dispensable for normal fertility but contribute modestly to fertilization.
Insights
The ADAM20 gene is not essential for mouse fertility, as knock-out males remain fertile in vivo. However, ADAM20, ADAM25, and ADAM39 genes modestly contribute to the fertilization process.
Area of Science:
- Reproductive Biology
- Genetics
- Molecular Biology
Background:
- A mutation in the ADAM20 gene has been linked to male infertility.
- ADAM20's precise role in mammalian fertilization remains unclear.
- ADAM20, ADAM25, and ADAM39 are homologous genes with potential overlapping functions.
Purpose of the Study:
- To investigate the function of ADAM20 in male fertility using a mouse model.
- To determine if ADAM25 and ADAM39 compensate for the loss of ADAM20.
- To elucidate the contribution of ADAM20, ADAM25, and ADAM39 to the fertilization process.
Main Methods:
- Generation of Adam20 knock-out (KO) mice.
- Assessment of in vivo fertility, sperm count, and morphology in Adam20-KO males.
- Performance of in vitro fertilization (IVF) assays.
- Generation of a triple KO mouse model lacking Adam20, Adam25, and Adam39.
Main Results:
- Adam20-KO males exhibited normal in vivo fertility and sperm parameters.
- Adam20-KO males showed reduced fertility in in vitro fertilization assays.
- Triple KO males displayed a phenotype identical to single Adam20-KO males, indicating no compensatory effect.
Conclusions:
- ADAM20, ADAM25, and ADAM39 are dispensable for normal male fertility in mice.
- These genes play a modest, non-essential role in the fertilization process.
- ADAM20 deficiency primarily impacts in vitro fertilization efficiency.
