Josephson Matthew P, Aliani Rana, Norris Megan L, Ochs Matthew E, Gujar Mahekta, Lundquist Erik A
Department of Molecular Biosciences, Program in Molecular, Cellular, and Developmental Biology, University of Kansas, Lawrence, Kansas 66046.
Department of Molecular Biosciences, Program in Molecular, Cellular, and Developmental Biology, University of Kansas, Lawrence, Kansas 66046
Genetics. 2017 Feb;205(2):737-748. doi: 10.1534/genetics.116.191957. Epub 2016 Dec 2.
During nervous system development, neurons and their progenitors migrate to their final destinations. In Caenorhabditis elegans, the bilateral Q neuroblasts and their descendants migrate long distances in opposite directions, despite being born in the same posterior region. QR on the right migrates anteriorly and generates the AQR neuron positioned near the head, and QL on the left migrates posteriorly, giving rise to the PQR neuron positioned near the tail. In a screen for genes required for AQR and PQR migration, we identified an allele of nfm-1, which encodes a molecule similar to vertebrate NF2/Merlin, an important tumor suppressor in humans. Mutations in NF2 lead to neurofibromatosis type II, characterized by benign tumors of glial tissues. Here we demonstrate that in C. elegans, nfm-1 is required for the ability of Q cells and their descendants to extend protrusions and to migrate, but is not required for direction of migration. Using a combination of mosaic analysis and cell-specific expression, we show that NFM-1 is required nonautonomously, possibly in muscles, to promote Q lineage migrations. We also show a genetic interaction between nfm-1 and the C. elegans Slit homolog slt-1, which encodes a conserved secreted guidance cue. Our results suggest that NFM-1 might be involved in the generation of an extracellular cue that promotes Q neuroblast protrusion and migration that acts with or in parallel to SLT-1 In vertebrates, NF2 and Slit2 interact in axon pathfinding, suggesting a conserved interaction of NF2 and Slit2 in regulating migratory events.
在神经系统发育过程中,神经元及其前体细胞迁移到它们的最终目的地。在秀丽隐杆线虫中,双侧的Q神经母细胞及其后代向相反方向长距离迁移,尽管它们都诞生于同一后端区域。右侧的QR向前迁移并产生位于头部附近的AQR神经元,左侧的QL向后迁移,产生位于尾部附近的PQR神经元。在一项针对AQR和PQR迁移所需基因的筛选中,我们鉴定出了nfm-1的一个等位基因,该基因编码一种与脊椎动物NF2/ Merlin相似的分子,后者是人类一种重要的肿瘤抑制因子。NF2突变会导致II型神经纤维瘤病,其特征是神经胶质组织出现良性肿瘤。在这里我们证明,在秀丽隐杆线虫中,nfm-1对于Q细胞及其后代伸出突起和迁移的能力是必需的,但对于迁移方向并非必需。通过结合镶嵌分析和细胞特异性表达,我们表明NFM-1非自主发挥作用,可能是在肌肉中,以促进Q系细胞迁移。我们还展示了nfm-1与秀丽隐杆线虫Slit同源物slt-1之间的遗传相互作用,slt-1编码一种保守的分泌型导向信号。我们的结果表明,NFM-1可能参与产生一种细胞外信号,该信号促进Q神经母细胞的突起和迁移,其作用方式与SLT-1协同或平行。在脊椎动物中,NF2和Slit2在轴突导向中相互作用,这表明NF2和Slit2在调节迁移事件方面存在保守的相互作用。