O'Connor P, Burnside B
J Cell Biol. 1981 Jun;89(3):517-24. doi: 10.1083/jcb.89.3.517.
Teleost retinal rods elongate when exposed to light. Elongation is mediated by a narrow necklike region called the myoid. In the cichlid Sarotherodon mossambicus, the rod inner segment (composed of the myoid with adjacent ellipsoid) increases in length from 12 micrometers in the dark to 41 micrometers in the light. Long light-adapted myoids contain longitudinally oriented microtubules and bundles of parallel 60-A filaments that we have identified as actin by their ability to bind myosin subfragment 1. In short dark-adapted myoids, only microtubules are recognizable. Colchicine experiments reveal that light-induced rod elongation can occur in the absence of myoid microtubules. Intraocular injections of colchicine at concentrations that disrupt virtually all rod myoid microtubules do not block rod elongation. However, rod elongation is blocked by intraocular injections of cytochalasin B or cytochalasin D. The hierarchy of effectiveness of these drugs is consistent with their effectiveness in inhibiting actin assembly and in disrupting other actin-dependent motile processes. On the basis of ultrastructural observations and the results of these inhibitor studies, we propose that the forces responsible for rod elongation are dependent not on microtubules but on actin filament assembly.
硬骨鱼的视网膜视杆在受到光照时会伸长。伸长是由一个称为肌样的狭窄颈部区域介导的。在丽鱼科的莫桑比克罗非鱼中，视杆内段（由肌样及其相邻的椭球体组成）的长度从黑暗中的12微米增加到光照下的41微米。长时间适应光照的肌样含有纵向排列的微管和平行的60埃细丝束，我们通过它们结合肌球蛋白亚片段1的能力将其鉴定为肌动蛋白。在短时间适应黑暗的肌样中，只能识别出微管。秋水仙碱实验表明，在没有肌样微管的情况下也能发生光诱导的视杆伸长。眼内注射几乎能破坏所有视杆肌样微管的秋水仙碱浓度并不会阻止视杆伸长。然而，眼内注射细胞松弛素B或细胞松弛素D会阻止视杆伸长。这些药物的有效性等级与其抑制肌动蛋白组装以及破坏其他肌动蛋白依赖性运动过程的有效性一致。基于超微结构观察和这些抑制剂研究的结果，我们提出导致视杆伸长的力不是依赖于微管，而是依赖于肌动蛋白丝的组装。
