Pan Jie, Ruest Louis-Bruno, Xu Suying, Wang Eugenia
Bloomfield Center for Research in Aging, Lady Davis Institute for Medical Research, Sir Mortimer B. Davis Jewish General Hospital and Department of Medicine, McGill University, Montréal, Canada.
Brain Res Dev Brain Res. 2004 Mar 22;149(1):1-8. doi: 10.1016/j.devbrainres.2003.10.011.
During early postnatal development, a switch occurs between eEF1A-1/EF-1alpha and eEF1A-2/S1, homologous peptide elongation factors, in brain, heart, and skeletal muscle; eEF1A-2/S1 becomes the major form expressed in maturity. By immunofluorescent labeling, we detected both homologues in the developing brains of wild-type and wasted mutant mice, carrying a deletion in the eEF1A-2/S1 gene; we found that brain expression of eEF1A-2/S1 protein is restricted to mature, terminally differentiated neurons, and coincides with the disappearance of eEF1A-1/EF-1alpha 20 days after birth. Furthermore, no elongation factor 1A is present in wasted mutant mice neurons following the developmental switch, indicating that the genetic regulation silencing eEF1A-1/EF-1alpha is still functional.
在出生后早期发育过程中,脑、心脏和骨骼肌中同源的肽链延长因子eEF1A - 1/EF - 1α和eEF1A - 2/S1之间会发生转换;eEF1A - 2/S1成为成熟时表达的主要形式。通过免疫荧光标记,我们在野生型和携带eEF1A - 2/S1基因缺失的消瘦突变小鼠的发育大脑中检测到了这两种同源物;我们发现eEF1A - 2/S1蛋白在大脑中的表达仅限于成熟的终末分化神经元,并且与出生后20天eEF1A - 1/EF - 1α的消失相一致。此外,在发育转换后,消瘦突变小鼠的神经元中不存在延长因子1A,这表明使eEF1A - 1/EF - 1α沉默的基因调控仍然有效。