Mosaic analysis of two genes that affect nervous system structure in Caenorhabditis elegans.
Mosaic analysis of two genes that affect nervous system structure in Caenorhabditis elegans.
复制标题
影响秀丽隐杆线虫神经系统结构的两个基因的镶嵌分析。
DOI：
10.1093/genetics/116.3.377
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发表时间：
1987
期刊：
影响因子：
3.3
通讯作者：
Herman,RK
中科院分区：
文献类型：
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作者：
Herman,RK
突变mec-4（e1611），由M. Chalfie，导致六个神经元的变性和死亡，称为微管细胞，介导野生型动物对轻触的反应。这些细胞中的两个，PLML和PLMR，这是负责在动物的尾巴轻触摸的反应，已监测在动物嵌合体的themec-4（e1611）突变的命运。这些结果与突变在其杀伤作用中表现为细胞自主的观点一致;特别是，没有一个神经元使PLML或PLMR的化学突触或间隙连接负责PLML或PLMR的死亡。基因剂量和显性试验的结果表明，ec-4（+）基因产物，这是野生型微管细胞功能所必需的，是由e1611突变改变成一种新的产品，杀死微管细胞。unc-3基因突变导致腹侧索运动神经元突起紊乱。镶嵌分析强烈提示unc-3（+）表达仅在运动神经元自身中是正常神经元发育所必需的。特别是，腹索周围的皮下组织不是func-3作用的主要焦点（在早期的研究中排除了体肌）。最后，镶嵌分析支持了早期的一个观点，即adaf-6突变引起的感觉缺陷局限于一个叫做鞘细胞的非神经元细胞。
The mutationmec-4(e1611), identified by M. Chalfie, leads to the degeneration and death of the six neurons, called the microtubule cells, that mediate the response of wild-type animals to light touch. The fates of two of these cells, PLML and PLMR, which are responsible for response to light touch in the tail of the animal, have been monitored in animals mosaic for themec-4(e1611) mutation. The results are consistent with the view that the mutation behaves cell autonomously in its killing effect; in particular, none of the neurons that make either chemical synapses or gap junctions to PLML or PLMR is responsible for the deaths of PLML or PLMR. The results of gene dosage and dominance tests suggest that themec-4(+) gene product, which is required for wild-type microtubule cell function, is altered by thee1611mutation into a novel product that kills the microtubule cells. Mutation in the geneunc-3leads to the derangement of the processes of the motor neurons of the ventral cord. Mosaic analysis strongly suggests thatunc-3(+) expression is required only in the motor neurons themselves for normal neuronal development. In particular, the hypodermis surrounding the ventral cord is not the primary focus ofunc-3action (body muscle was excluded in earlier work). Finally, the mosaic analysis supports an earlier suggestion that a sensory defect caused by adaf-6mutation is localized to a non-neuronal cell called the sheath cell.