Bachnou N, Saule S, Dieterlen-Lievre F
Institut d'Embryologie Cellulaire et Moléculaire du CNRS et du College de France, Lille, France.
Int J Dev Biol. 1996 Apr;40(2):491-7.
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 growing heart rhabdomyomas (induced by v-myc alone) and within these tumors secondarily appearing cartilage nodules (Bachnou et al., Oncogene 6: 1041-1047, 1991). Here we report that v-erbA can be replaced by thyroid deficiency. When decapitated embryos were inoculated with virus MC29 (v-myc alone) or when v-myc inoculated embryos were treated with thiourea, 100% of the embryos reaching E17 to E19 displayed tumoral hearts 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, versus about 70% affected when either v-myc or MAHEVA were inoculated. Thyroid deficiency did not alter the species-specific character of transdifferentiation, since only chick but not quail embryos developed cartilage nodules after thyroidectomy or MAHEVA infection.
我们之前已经表明，v-myc与v-erbA的结合（MAHEVA构建体）导致在E3期接种的鸡胚中出现特定表型。该表型包括快速生长的心脏横纹肌瘤（由单独的v-myc诱导），并且在这些肿瘤中继而出现软骨结节（Bachnou等人，《癌基因》6: 1041 - 1047, 1991）。在此我们报告，v-erbA可被甲状腺功能减退所替代。当给断头胚胎接种病毒MC29（单独的v-myc）时，或者当给接种v-myc的胚胎用硫脲处理时，所有发育到E17至E19期的胚胎都显示出带有软骨结节的肿瘤性心脏。因此，我们报告了体内证据，表明v-erbA通过拮抗甲状腺激素的作用发挥功能。值得注意的是，甲状腺功能减退使胚胎对v-myc的作用更敏感，因为100%的胚胎都发育出心脏横纹肌瘤和软骨结节，而接种v-myc或MAHEVA时约70%的胚胎受到影响。甲状腺功能减退并未改变转分化的物种特异性特征，因为甲状腺切除或MAHEVA感染后，只有鸡胚而非鹌鹑胚发育出软骨结节。
