Fundele R, Illmensee K, Jägerbauer E M, Fehlau M, Krietsch W K
Laboratoire de Différenciation cellulaire, Ecole de Médecine, Genève 4, Switzerland.
Differentiation. 1987;35(1):31-6. doi: 10.1111/j.1432-0436.1987.tb00148.x.
Enzyme activities of X-linked phosphoglycerate kinase (PGK-1) and autosomal glucose phosphate isomerase (GPI-1) were determined in intact mouse blastocysts and isolated inner cell masses (ICMs). Blastocysts were recovered from the uterus on day 4 of gestation and cultured overnight in vitro. ICMs were isolated by treatment with calcium ionophore A23187. On day 4, approximately 35% of the total activity of both PGK-1 and GPI-1 was located in the ICM. After overnight culture, the PGK-1 activity of the whole blastocyst nearly doubled, due to the activation of only the maternally derived gene coding for PGK-1. In the ICM, however, a pronounced decrease of PGK-1 activity was measured: only 10% of the total PGK-1 activity was measured in the ICM on day 5. In contrast to PGK-1, GPI-1 activity of the intact blastocyst remained stable from day 4 to day 5. In the ICM, the GPI-1 activity did decline, but to a lesser extent than PGK-1 activity: 20% of total GPI-1 activity was found in the ICM on day 5. These results, when compared with the data of Handyside and Hunter, suggest that the decline in GPI-1 activity in the ICM is due to a change in the ratio of trophectoderm (TE) to ICM cells. The greater reduction of PGK-1 activity in the ICM cannot, however, be explained solely by this mechanism. To explain the observed additional decrease, we postulate that Pgk-1 is not activated in the ICM prior to day 6. This implies that on day 4 maternal Pgk-1 is activated in the TE exclusively.
在完整的小鼠囊胚和分离的内细胞团（ICM）中测定了X连锁磷酸甘油酸激酶（PGK-1）和常染色体葡萄糖磷酸异构酶（GPI-1）的酶活性。在妊娠第4天从子宫中回收囊胚，并在体外培养过夜。通过用钙离子载体A23187处理来分离ICM。在第4天，PGK-1和GPI-1的总活性中约35%位于ICM中。过夜培养后，整个囊胚的PGK-1活性几乎翻倍，这是由于仅编码PGK-1的母源基因被激活。然而，在ICM中，PGK-1活性显著下降：在第5天，ICM中仅检测到总PGK-1活性的10%。与PGK-1不同，完整囊胚的GPI-1活性从第4天到第5天保持稳定。在ICM中，GPI-1活性确实下降了，但下降程度小于PGK-1活性：在第5天，ICM中发现总GPI-1活性的20%。这些结果与汉迪赛德和亨特的数据相比，表明ICM中GPI-1活性的下降是由于滋养外胚层（TE）与ICM细胞比例的变化。然而，ICM中PGK-1活性更大程度的降低不能仅用这种机制来解释。为了解释观察到的额外下降，我们假设在第6天之前Pgk-1在ICM中未被激活。这意味着在第4天，母源Pgk-1仅在TE中被激活。
