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J Neurobiol. 1993 Jul;24(7):971-84.

Dendritic reduction in Passover, a Drosophila mutant with a defective giant fiber neuronal pathway.

Author information

1
Department of Anatomy and Neurobiology, Medical College of Pennsylvania, Philadelphia 19129.

Abstract

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.

PMID:
8228974
DOI:
10.1002/neu.480240710
[Indexed for MEDLINE]

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