Williams D S, Linberg K A, Vaughan D K, Fariss R N, Fisher S K
Neurosciences Research Program, University of California, Santa Barbara 93106.
J Comp Neurol. 1988 Jun 8;272(2):161-76. doi: 10.1002/cne.902720202.
Morphogenesis of photoreceptor outer segment disks appears to occur by an evagination of the ciliary plasma membrane (Steinberg et al., J Comp Neurol 190:501-519, '80). We tested if polymerized actin (F-actin) was necessary for the regulation of this postulated process by incubating Xenopus eyecups with 5 or 25 microM cytochalasin D for 6-28 hours. During the second hour, the incubation medium contained 3H-leucine. Both concentrations of cytochalasin resulted in: 1) dissolution of the rhodamine-phalloidin labeling pattern of photoreceptors, and 2) collapse of the calycal processes (which are normally filled with actin filaments) and disappearance of the inner segment microfilaments. In addition, the few most basal rod and cone outer segment disks appeared several times their normal diameter. These oversized disks had incorporated 3H-leucine and extended along the margin of the outer or inner segment. The nature of the overgrown disks is consistent only with a morphogenetic process involving evaginations of the ciliary plasma membrane. Deregulation by cytochalasin D was manifest by excessive growth of a few nascent disks rather than normal growth of many. Therefore, the normal network of actin filaments is apparently not necessary for continued evagination of the membrane, but it does seem to be an essential part of the mechanism that initiates the evagination of the ciliary plasma membrane and/or the mechanism that controls how far nascent disks grow.
光感受器外段盘的形态发生似乎是通过睫状质膜的内陷来实现的(斯坦伯格等人,《比较神经学杂志》190:501 - 519,1980年)。我们通过将非洲爪蟾眼杯与5或25微摩尔的细胞松弛素D孵育6 - 28小时,来测试聚合肌动蛋白(F - 肌动蛋白)对于这一假定过程的调节是否必要。在第二个小时,孵育培养基中含有3H - 亮氨酸。两种浓度的细胞松弛素都导致了:1)光感受器的罗丹明 - 鬼笔环肽标记模式消失,以及2)萼状突起(通常充满肌动蛋白丝)塌陷和内段微丝消失。此外,少数最基部的视杆和视锥外段盘出现了几倍于正常直径的情况。这些超大的盘掺入了3H - 亮氨酸,并沿着外段或内段的边缘延伸。这些过度生长的盘的性质仅与涉及睫状质膜内陷的形态发生过程一致。细胞松弛素D导致的调节失控表现为少数新生盘过度生长,而不是许多盘的正常生长。因此,肌动蛋白丝的正常网络显然对于膜的持续内陷不是必需的,但它似乎确实是启动睫状质膜内陷的机制和/或控制新生盘生长程度的机制的重要组成部分。