Induction of telomerase activity in v-myc-transformed avian cells

Telomerase activity is detectable in the majority of tumors or immortalized cell lines, but is repressed in most normal human somatic cells. It is gen erally assumed that reactivation of telomerase prevents the erosion of chro mosome ends which occurs in cycling cells and, hence, hinders cellular repl icative senescence. Here, we show that the expression of v-Myc oncoprotein by retroviral infection of telomerase-negative embryonal quail myoblasts an d chicken neuroretina cells is sufficient for reactivating telomerase activ ity, earlier than telomere shortening could occur. Furthermore, the use of a conditional v-Myc-estrogen receptor protein (v-MycER) causes estrogen-dep endent expression of detectable levels of telomerase activity in recently i nfected chick embryo fibroblasts and neuroretina cells. We conclude that th e high levels of telomerase activity in v-Myc-expressing avian cells are no t the mere consequence of transformation or of a differentiative block, sin ce v-Src tyrosine kinase, which prevents terminal differentiation and promo tes cell transformation, fails to induce telomerase activity.