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Mitochondrial dysfunction caused by targeted deletion of Mfn1 does not result in telomere shortening in oocytes

Published online by Cambridge University Press:  22 June 2022

Mauro Cozzolino Open the ORCID record for Mauro Cozzolino [Opens in a new window]  and
Emre Seli
Mauro Cozzolino
Affiliation:
Department of Obstetrics, Gynecology, and Reproductive Sciences, Yale School of Medicine, New Haven, Connecticut, USA Universidad Rey Juan Carlos, Madrid, Spain IVIRMA, IVI Foundation, Valencia, Spain
Emre Seli*
Affiliation:
Department of Obstetrics, Gynecology, and Reproductive Sciences, Yale School of Medicine, New Haven, Connecticut, USA IVIRMA New Jersey, Basking Ridge, New Jersey, USA
*
Author for correspondence: Emre Seli. Department of Obstetrics, Gynecology, and Reproductive Sciences, Yale School of Medicine, 310 Cedar Street LSOG 304B, New Haven, CT 06520–8063, USA. Tel: +1 203 785 7873. Fax: +1 203 785 7819. E-mail: emre.seli@yale.edu
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Summary

Telomere shortening during oocyte growth and development is related to reproductive ageing and infertility. The main mechanism involved in the maintenance of telomeres is based on telomerase activity, a specialized enzyme complex, which is capable of adding TTAGGG repeats at the ends of the chromosomes. Mitochondrial dysfunction may cause progressive shortening of telomeres by promoting the generation of reactive oxygen species. Mitofusin-1 is a protein required for mitochondrial fusion. Mice with the mitofusin-1 (Mfn1) deletion in the oocyte are characterized by accelerated follicular depletion and infertility, associated with defective oocyte maturation and follicular development. We hypothesized whether mitochondrial dysfunction in oocytes with targeted deletion of Mfn1 causes telomere shortening. We analyzed telomere length in oocyte and somatic cells in 3-, 6- and 9-month-old Mfn1−/− and wild-type mice. Immunofluorescence in oocyte mice of TRF1 and H2A.X was assessed to evaluate the interplay between the end-protection functions and the response to DNA damage occurring inside the telomeric repeats. Mitochondrial dysfunction due to the deletion of Mfn1 does not seem to affect telomere length in mouse oocytes.

Keywords

Mitochondrial dysfunctiontelomere lengthreactive oxygen speciesMitofusin-1
Type
Short Communication
Information
Zygote , Volume 30 , Issue 5 , October 2022 , pp. 735 - 737
Copyright
© The Author(s), 2022. Published by Cambridge University Press

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References

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