Harper M I, Monk M
J Embryol Exp Morphol. 1983 Apr;74:15-28.
This paper presents evidence that maternal mRNA is responsible for the early increase in HPRT activity in preimplantation mouse embryos. Increase of HPRT activity is demonstrable from as early as 6 h postfertilization when there is barely detectable synthesis of embryonic RNA. The increase is sensitive to cycloheximide and thus requires protein synthesis, whereas it is insensitive to alpha-amanitin and therefore independent of mRNA synthesis. These results suggest that translation of HPRT occurs on pre-existing maternal mRNA. Embryo-coded HPRT activity is detectable by the 4- to 8-cell stage when the increase in HPRT activity becomes sensitive to alpha-amanitin. The transition from maternal- to embryo-coded enzyme activity is completed by the time of compaction. At this stage there is an unexplained yet reproducible loss of HPRT activity. Other maternally-inherited enzymes show a marked degradation occurring at a similar time. It is possible that the enzyme degradation observed reflects some common mechanism directing the changeover from maternally-derived to embryonically-derived enzymes.
本文提供的证据表明,母体mRNA负责着床前小鼠胚胎中次黄嘌呤磷酸核糖转移酶(HPRT)活性的早期增加。早在受精后6小时就能证明HPRT活性增加,此时胚胎RNA的合成几乎检测不到。这种增加对放线菌酮敏感,因此需要蛋白质合成,而对α-鹅膏蕈碱不敏感,因此与mRNA合成无关。这些结果表明,HPRT的翻译发生在预先存在的母体mRNA上。当HPRT活性的增加对α-鹅膏蕈碱敏感时,在4至8细胞阶段可检测到胚胎编码的HPRT活性。从母体编码的酶活性到胚胎编码的酶活性的转变在致密化时完成。在这个阶段,HPRT活性出现了无法解释但可重复的损失。其他母体遗传的酶也在类似时间出现明显降解。观察到的酶降解可能反映了一些指导从母体来源的酶向胚胎来源的酶转变的共同机制。