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Research Article |
1 Dipartimento di Sanita' Pubblica e Biologia Cellulare, Sezione di Anatomia,
Rome, Italy
2 Istituto Dermopatico dell'Immacolata (IDI, IRCCS), Rome, Italy
3 Dipartimento di Neuroscienze, Universita' di Roma Tor Vergata, Rome,
Italy
* Author for correspondence (e-mail: dolci{at}uniroma2.it )
Accepted 28 January 2002
The discovery of sterility in the descendants of telomerasenull mutant mice, owing to the lack of spermatogonia proliferation, has drawn attention to the role of telomerase activity in mouse spermatogenesis. Since spermatogonia proliferation is under Kitl control, we explored its possible role in the regulation of telomerase activity. We show that Kitl induces telomerase activity in mitotic spermatogonia and increases the mRNA levels of both the catalytic subunit form and the telomerase RNA template. The increase of telomerase activity by Kitl is blocked by the presence of the PI3K inhibitor LY294002. Kit-positive proliferating male primordial germ cells (PGCs) show low levels of telomerase activity, but they increase telomerase activity upon Kitl stimulation. Diplotene-arrested growing oocytes that reexpress Kit do not increase telomerase activity upon Kitl stimulation. Our data suggest that the induction of telomerase by Kitl may contribute to the self-renewing potential of male germ cells and of PGCs.
Key words: Kitl, Kit, Telomerase, Germ cells, Meiosis, Proliferation, PI3K
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