Article révisé par les pairs
Résumé : Mouse embryos were treated from the 2-cell stage onwards with methylglyoxal-Bis (guanylhydrazone) MGBG), a potent inhibitor of spermidine and spermine synthesis. The early nucleolar reactivation, revealed by both AgNO3 staining and ultrastructural autoradiography, takes place in a similar way in both control and treated embryos. On the other hand, the well known dramatic increase in uridine incorporation together with the further nucleolar maturation, taking place before the onset of blastocyst formation, are reversibly inhibited in the quiescent 8-10 cell stage MGBG-treated embryos. After removal of the drug, the genetic activation is restored with a delay perfectly superposable to that induced in the cavitation process. This confirms that cavitation is strictly dependent on molecular differentiation and suggests that polyamines are involved in this process. These results also support the hypothesis of a desynchronisation between chromosome replication progress and cytoplasmic maturation (molecular differentiation) as an explanation for the lower cell number of the 'delayed nascent blastocysts' resulting from a transient treatment with MGBG.