Forer A
Can J Biochem Cell Biol. 1985 Jun;63(6):585-98. doi: 10.1139/o85-077.
Chromosomes move towards spindle poles because of force produced by chromosomal spindle fibres. I argue that actin is involved in producing this force. Actin is present in chromosomal spindle fibres, with consistent polarity. Physiological experiments using ultraviolet microbeam irradiations suggest that the force is due to an actin and myosin (or myosin-equivalent) system. Other physiological experiments (using inhibitors in "leaky" cells or antibodies injected into cells) that on the face of it would seem to rule out actin and myosin on closer scrutiny do not really do so at all. I argue that in vivo the "on" ends of chromosomal spindle fibre microtubules are at the kinetochores; I discuss the apparent contradiction between this conclusion and those from experiments on microtubules in vitro. From what we know of treadmilling in microtubules in vitro, the poleward movements of irradiation-induced areas of reduced birefringence (arb) can not be explained as treadmilling of microtubules: additional assumptions need to be made for arb movements toward the pole to be due to treadmilling. If arb movement does indeed represent treadmilling along chromosomal spindle fibre microtubules, treadmilling continues throughout anaphase. Thus I suggest that chromosomal spindle fibres shorten in anaphase not because polymerization is stopped at the kinetochore (the on end), as previously assumed, but rather because there is increased depolymerization at the pole (the "off" end).
染色体向纺锤体两极移动是由于染色体纺锤体纤维产生的力。我认为肌动蛋白参与了这种力的产生。肌动蛋白存在于染色体纺锤体纤维中，具有一致的极性。使用紫外线微束照射的生理学实验表明，这种力是由于肌动蛋白和肌球蛋白（或类似肌球蛋白的物质）系统。其他生理学实验（在“渗漏”细胞中使用抑制剂或向细胞中注射抗体），表面上似乎排除了肌动蛋白和肌球蛋白，但仔细审查后根本并非如此。我认为在体内，染色体纺锤体纤维微管的“正”端位于动粒上；我讨论了这一结论与体外微管实验结论之间明显的矛盾。根据我们对体外微管踏车行为的了解，照射诱导的双折射降低区域（arb）向极的移动不能解释为微管的踏车行为：要使arb向极的移动归因于踏车行为，需要做出额外的假设。如果arb移动确实代表沿着染色体纺锤体纤维微管的踏车行为，那么踏车行为在整个后期都会持续。因此我认为，染色体纺锤体纤维在后期缩短，不是因为如先前假设的那样，聚合在动粒（正端）处停止，而是因为在极（“负”端）处解聚增加。
