Johnson T C, Belytschko G
Proc Natl Acad Sci U S A. 1969 Mar;62(3):844-51. doi: 10.1073/pnas.62.3.844.
The loss of protein synthesis during early mouse-brain development was shown to be the result, at least in part, of the inability of microsomes obtained from more mature neural tissue to participate in rapid polypeptide synthesis. The loss of brain microsomal activity was observed shortly after birth and continued until the animals were approximately ten days old. Despite the difference in synthetic activity, sucrose gradient profiles of microsomes and polyribosomes from young and more mature brain tissue were quite similar. The loss in protein synthesis was shown to be independent of available mRNA and not attributable to aminoacyl-RNA synthetases and tRNA binding activity.
在小鼠脑发育早期,蛋白质合成的丧失至少部分是由于从更成熟神经组织获得的微粒体无法参与快速多肽合成所致。出生后不久就观察到脑微粒体活性的丧失,并持续到动物大约十天大。尽管合成活性存在差异,但来自幼龄和更成熟脑组织的微粒体和多聚核糖体的蔗糖梯度图谱非常相似。蛋白质合成的丧失与可用的mRNA无关,也不归因于氨酰基-RNA合成酶和tRNA结合活性。