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线虫秀丽隐杆线虫中的突变感觉纤毛。

Mutant sensory cilia in the nematode Caenorhabditis elegans.

作者信息

Perkins L A, Hedgecock E M, Thomson J N, Culotti J G

出版信息

Dev Biol. 1986 Oct;117(2):456-87. doi: 10.1016/0012-1606(86)90314-3.

Abstract

Eight classes of chemosensory neurons in C. elegans fill with fluorescein when living animals are placed in a dye solution. Fluorescein enters the neurons through their exposed sensory cilia. Mutations in 14 genes prevent dye uptake and disrupt chemosensory behaviors. Each of these genes affects the ultrastructure of the chemosensory cilia or their accessory cells. In each case, the cilia are shorter or less exposed than normal, suggesting that dye contact is the principal factor under selection. Ten genes affect many or all of the sensory cilia in the head. The daf-19 (m86) mutation eliminates all cilia, leaving only occasional centrioles in the dendrites. The cilia in che-13 (e1805), osm-1 (p808), osm-5 (p813), and osm-6 (p811) mutants have normal transition zones and severely shortened axonemes. Doublet-microtubules, attached to the membrane by Y links, assemble ectopically proximal to the cilia in these mutants. The amphid cilia in che-11 (e1810) are irregular in diameter and contain dark ground material in the middle of the axonemes. Certain mechanocilia are also affected. The amphid cilia in che-10 (e1809) apparently degenerate, leaving dendrites with bulb-shaped endings filled with dark ground material. The mechanocilia lack striated rootlets. Cilia defects have also been found in che-2, che-3, and daf-10 mutants. The osm-3 (p802) mutation specifically eliminates the distal segment of the amphid cilia. Mutations in three genes affect sensillar support cells. The che-12 (e1812) mutation eliminates matrix material normally secreted by the amphid sheath cell. The che-14 (e1960) mutation disrupts the joining of the amphid sheath and socket cells to form the receptor channel. A similar defect has been observed in daf-6 mutants. Four additional genes affect specific classes of ciliated sensory neurons. The mec-1 and mec-8 (e398) mutations disrupt the fasciculation of the amphid cilia. The cat-6 (e1861) mutation disrupts the tubular bodies of the CEP mechanocilia. A cryophilic thermotaxis mutant, ttx-1 (p767), lacks fingers on the AFD dendrite, suggesting this neuron is thermosensory.

摘要

当活体秀丽隐杆线虫被置于染料溶液中时,其八类化学感受神经元会充满荧光素。荧光素通过暴露的感觉纤毛进入神经元。14个基因的突变会阻止染料摄取并破坏化学感受行为。这些基因中的每一个都会影响化学感受纤毛或其辅助细胞的超微结构。在每种情况下,纤毛都比正常的短或暴露程度更低,这表明染料接触是选择的主要因素。10个基因会影响头部的许多或所有感觉纤毛。daf-19(m86)突变会消除所有纤毛,在树突中仅偶尔留下中心粒。che-13(e1805)、osm-1(p808)、osm-5(p813)和osm-6(p811)突变体中的纤毛具有正常的过渡区,轴丝严重缩短。通过Y形连接附着在膜上的双微管在这些突变体中异位组装在纤毛近端。che-11(e1810)中的两性纤毛直径不规则,轴丝中部含有暗物质。某些机械感受纤毛也受到影响。che-10(e1809)中的两性纤毛明显退化,留下充满暗物质的球状末端树突。机械感受纤毛缺乏横纹小根。在che-2、che-3和daf-10突变体中也发现了纤毛缺陷。osm-3(p802)突变特异性地消除两性纤毛的远端部分。三个基因的突变会影响感觉器支持细胞。che-12(e1812)突变会消除两性鞘细胞正常分泌的基质物质。che-14(e1960)突变会破坏两性鞘细胞和套接细胞形成受体通道的连接。在daf-6突变体中也观察到了类似的缺陷。另外四个基因会影响特定类别的纤毛感觉神经元。mec-1和mec-8(e398)突变会破坏两性纤毛的成束。cat-6(e1861)突变会破坏CEP机械感受纤毛的管状小体。一个嗜冷趋温突变体ttx-1(p767)在AFD树突上缺乏指状结构,表明该神经元具有温度感受功能。

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