AN IDENTICAL EFFECT MEDIATED BY THYROID-DEFICIENCY OR ONCOGENE V-ERBAIN THE CHICK-EMBRYO

We have shown earlier that the association of v-myc and v-erbA (MAHEVA construct) is responsible for the appearance of a specific phenotype in chick embryos inoculated at E3. This phenotype comprises rapidly gr owing heart rhabdomyomas (induced by v-myc alone) and within these tum ors secondarily appearing cartilage nodules (Bachnou at al., Oncogene 6: 1041-1047, 1991). Here we report that v-erbA can be replaced by thy roid deficiency. When decapitated embryos were inoculated with virus M C29 (v-myc alone) or when v-myc inoculated embryos were treated with t hiourea, 100% of the embryos reaching E17 to E19 displayed tumoral hea rts bearing cartilage nodules. We thus report in vivo evidence that v- erbA acts by antagonizing the effects of thyroid hormones. Remarkably, thyroid deficiency rendered embryos more sensitive to the effect of v -myc, since 100% developed heart rhabdomyomas and cartilage nodules, v ersus about 70% affected when either v-myc or MAHEVA were inoculated. Thyroid deficiency did not alter the species-specific character of tra nsdifferentiation, since only chick but not quail embryos developed ca rtilage nodules after thyroidectomy or MAHEVA infection.