Baird D H, Koto M, Wyman R J
Department of Anatomy and Neurobiology, Medical College of Pennsylvania, Philadelphia 19129.
J Neurobiol. 1993 Jul;24(7):971-84. doi: 10.1002/neu.480240710.
The jump response to a light-off startle stimulus in Drosophila melanogaster occurs when the Giant Fiber (GF), a neuron descending from the brain to the thorax, drives the jump (tergotrochanteral) muscle motorneuron (TTMn). Nonjumping mutants have been isolated in which this response is disrupted. Flies bearing the X-chromosome mutation Passover (Pas) fail to jump in response to a light-off stimulus, and electrical stimulation of the GF in the brain no longer elicits the normal response in the TTM. We have used retrograde HRP labelling to examine the TTMn motorneuron in wild-type flies and in a variety of newly identified Pas alleles. In wild type the medial branch (MB) of the TTMn has an extensive region of apposition with the GF. In Pas alleles, there is a general reduction in anterior-posterior (A-P) extent of the medial branch but not of the posterior branch. Nevertheless, Pas alleles usually leave the TTMn close enough to the GF so that contact would not be precluded. In flies carrying a particular deficiency of Pas, Df(1) 16-3-22, including Pas/Df(1) 16-3-22 heterozygotes, there can be extensive growth of the medial-branch including a contralateral projection; these heterozygotes have more than the normal amount of overlap between the GF and the TTMn. This phenotype, originally ascribed to Pas mutants, is associated with Df(1) 16-3-22, but not with other deletions of the Pas gene. The driving of the TTMn by the GF is defective in mutant genotypes with extensive medial branches as well as in mutants where GF-TTMn contact is reduced. The fact that the TTMn grows into its normal synaptic region in mutant genotypes, but the GF pathway functions abnormally suggests that pathfinding by the TTMn is not impaired. It is more likely that the Pas mutation disrupts cell recognition, synaptogenesis, or synaptic function in the TTMn or its presynaptic partners.
在黑腹果蝇中，对熄灯惊吓刺激的跳跃反应发生在巨纤维（GF）驱动跳跃（转节间）肌肉运动神经元（TTMn）时，GF是一种从大脑延伸至胸部的神经元。已分离出非跳跃突变体，其这种反应受到破坏。携带X染色体突变逾越节（Pas）的果蝇对熄灯刺激无跳跃反应，并且对大脑中的GF进行电刺激不再能在TTM中引发正常反应。我们使用逆行HRP标记来检查野生型果蝇以及各种新鉴定的Pas等位基因中的TTMn运动神经元。在野生型中，TTMn的内侧分支（MB）与GF有广泛的并置区域。在Pas等位基因中，内侧分支的前后（A-P）范围普遍减小，但后分支没有。然而，Pas等位基因通常使TTMn与GF保持足够近的距离，因此不会排除接触。在携带特定Pas缺失的果蝇Df(1) 16 - 3 - 22中，包括Pas/Df(1) 16 - 3 - 22杂合子，内侧分支可能会广泛生长，包括对侧投射；这些杂合子在GF和TTMn之间有比正常更多的重叠。这种最初归因于Pas突变体的表型与Df(1) 16 - 3 - 22相关，但与Pas基因的其他缺失无关。在具有广泛内侧分支的突变基因型以及GF - TTMn接触减少的突变体中，GF对TTMn的驱动存在缺陷。在突变基因型中TTMn生长到其正常突触区域，但GF通路功能异常，这一事实表明TTMn的路径寻找未受损。更有可能的是，Pas突变破坏了TTMn或其突触前伙伴中的细胞识别、突触形成或突触功能。
