Lack of Rev7 function results in development of tubulostromal adenomas in mouse ovary

Abdolrahim Abbasi, Maryam Khalaj, Kouyou Akiyama, Yoshiyuki Mukai, Hirokazu Matsumoto, Tomas J. Acosta, Neveen Said, Midori Yoshida, Tetsuo Kunieda

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Abstract

Rev7 is a subunit of Polζ, one of the translesion DNA synthesis (TLS) polymerases involved in DNA damage repair. We recently found that Rev7 is also essential for germ cell development in mouse. In the present study, we found the development of ovarian tumors in Rev7 mutant mouse, suggesting the involvement of TLS deficiency in the etiology of ovarian tumor. The Rev7 mutant mice showed complete lack of oocytes and follicles in the ovary. The lack of follicles causes a significant increase of gonadotropin level and an increase in the proliferation of ovarian cells. As a result, the weight of the ovaries of Rev7 mutant mice increased with age and they developed tubulostromal adenomas. However, the remarkable overgrowth of ovaries occurred after gonadotropin level decreases at older ages, suggesting gonadotropin-independent progression of the ovarian tumors. In addition, the Rev7 mutant fibroblasts and ovarian cells showed significant accumulation of DNA damage. These findings suggest that not only increased gonadotropin levels but also lack of DNA damage repair function could be responsible for the development of ovarian tumors in the Rev7 mutant mouse.

Original languageEnglish
Pages (from-to)19-25
Number of pages7
JournalMolecular and Cellular Endocrinology
Volume412
DOIs
Publication statusPublished - Sep 5 2015

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Keywords

  • Gonadotropin
  • Ovarian tumors
  • Rev7
  • Translesion DNA polymerase

ASJC Scopus subject areas

  • Endocrinology
  • Molecular Biology
  • Biochemistry

Cite this

Abbasi, A., Khalaj, M., Akiyama, K., Mukai, Y., Matsumoto, H., Acosta, T. J., Said, N., Yoshida, M., & Kunieda, T. (2015). Lack of Rev7 function results in development of tubulostromal adenomas in mouse ovary. Molecular and Cellular Endocrinology, 412, 19-25. https://doi.org/10.1016/j.mce.2015.05.022