Hua Y, Zhou J
Department of Medicine, Program in Neuroscience, University of Massachusetts, Medical School, 364 Plantation Street, LRB 325, Worcester, Massachusetts 01605, USA.
Cell Mol Life Sci. 2004 Oct;61(19-20):2658-63. doi: 10.1007/s00018-004-4300-z.
The survival of motor neuron ( SMN1) gene product, SMN, is detected both in the cytoplasm and in nuclear gems and cajal bodies. We show here that SMN exon 6 is essential both for formation of its nuclear foci and for its cytoplasmic localization. However, exon 7 inhibits the formation of SMN nuclear foci but promotes SMN cytoplasmic localization. More interestingly, we find that a random C-terminal tag of five or more amino acids downstream of exon 6 is sufficient to inhibit the occurrence of multiple nuclear foci and to promote cytoplasmic localization of SMNDelta7, the primary product of the SMN2 gene. Moreover, SMNDelta7 proteins that bear spinal muscular atrophy mutations in exon 6 either showed defects in nuclear foci formation or enhanced cytoplasmic localization. We conclude that exon 6 and exon 7 synergistically regulate SMN distribution that may require specific exon 6 motifs but is independent of specific sequences in exon 7.
运动神经元存活基因(SMN1)的产物SMN在细胞质以及核宝石和卡哈尔体中均有检测到。我们在此表明,SMN外显子6对于其核灶的形成及其细胞质定位均至关重要。然而,外显子7会抑制SMN核灶的形成,但会促进SMN的细胞质定位。更有趣的是,我们发现外显子6下游五个或更多氨基酸的随机C末端标签足以抑制多个核灶的出现,并促进SMN2基因的主要产物SMNDelta7的细胞质定位。此外,在外显子6中带有脊髓性肌萎缩症突变的SMNDelta7蛋白要么在核灶形成中表现出缺陷,要么增强了细胞质定位。我们得出结论,外显子6和外显子7协同调节SMN的分布,这可能需要特定的外显子6基序,但与外显子7中的特定序列无关。