Ono K, Tomasiewicz H, Magnuson T, Rutishauser U
Department of Neurosciences, Case Western Reserve University, Cleveland, Ohio 44106.
Neuron. 1994 Sep;13(3):595-609. doi: 10.1016/0896-6273(94)90028-0.
The mutation of N-CAM in mice produces a phenotype dominated by an undersized olfactory bulb and accumulation of precursors in the subependymal layer. We demonstrate here that this defect can be duplicated by injection of an enzyme that specifically destroys the polysialic acid (PSA) moiety associated with N-CAM. Studies of BrdU-labeled and pyknotic cells suggest that this defect reflects a decrease in the rostral migration of olfactory precursors and not a change in the proliferation or rate of death of these cells. In addition to their ectopic location, these cells had fewer growth cone-like processes oriented along the migration route. In contrast to tangential movement, radial migration of granule cells in the olfactory bulb was not affected by loss of PSA. These results support the proposed role for PSA in cell translocation, discriminate between different mechanisms of cell migration, and provide insight as to the nature of the N-CAM mutant phenotype.
小鼠中N-CAM的突变产生的表型主要表现为嗅球过小以及室管膜下层前体细胞的积累。我们在此证明，通过注射一种能特异性破坏与N-CAM相关的多唾液酸（PSA）部分的酶，可重现这种缺陷。对BrdU标记细胞和固缩细胞的研究表明，这种缺陷反映出嗅球前体细胞向头端迁移的减少，而非这些细胞增殖或死亡速率的改变。除了异位定位外，这些细胞沿迁移路线定向的生长锥样突起较少。与切向运动不同，嗅球中颗粒细胞的径向迁移不受PSA缺失的影响。这些结果支持了PSA在细胞移位中所起的作用，区分了不同的细胞迁移机制，并为N-CAM突变体表型的本质提供了见解。
