Disease relevance of ss

• Loss-of-function mutations in the spineless-aristapedia gene of Drosophila (ssa mutants) cause transformations of the distal antenna to distal second leg, deletions or fusions of the tarsi from all three legs, a general reduction in bristle size, and sterility [1].

High impact information on ss

• In loss-of-function ss mutants, class I and II da neurons, which are normally characterized by their simple dendrite morphologies, elaborate more complex arbors, whereas the normally complex class III and IV da neurons develop simpler dendritic arbors [2].
• In both the antenna and leg, ss expression is shown to depend on Distal-less (Dll), a master regulator of ventral appendage formation [3].
• Loss-of-function alleles of ss cause three major phenotypes: transformation of distal antenna to leg, deletion of distal leg (tarsal) structures, and reduction in size of most bristles [3].
• We report the molecular characterization of the spineless (ss) gene of Drosophila, and present evidence that it plays a central role in defining the distal regions of both the antenna and leg. ss encodes the closest known homolog of the mammalian dioxin receptor, a transcription factor of the bHLH-PAS family [3].
• In the tarsus, ss is expressed only early, and is required for later expression of the tarsal gene bric à brac (bab) [3].

Biological context of ss

• During embryogenesis, Tgo is localized to the nucleus at sites of ss expression [4].
• Identification of this phenotype, together with observed variations in the extent of the fusion of tarsal segments in the legs of different segments, raised the possibility that ssa interacts with homeotic genes controlling the identity of segments [5].
• The spineless and tango were essential for suppressing the basal enhancer activation in early third instar [6].
• The autonomous and nonautonomous apoptosis caused by ss is regulated by a novel leucine-rich repeat family transmembrane protein, Fish-lips (Fili) that interacts with surrounding normal cells [7].
• Previous mapping studies of the AHR have demonstrated that the PAS domain contains sequences required for ligand recognition, dimerization, and interaction with the 90-kDa heat shock protein [8].

Anatomical context of ss

• The development of the sensory neuron pattern in the antennal disc of wild-type and mutant (lz3, ssa) Drosophila melanogaster [9].

Regulatory relationships of ss

• Wing-to-Leg homeosis by spineless causes apoptosis regulated by Fish-lips, a novel leucine-rich repeat transmembrane protein [7].

Other interactions of ss

• The spineless-aristapedia and tango bHLH-PAS proteins interact to control antennal and tarsal development in Drosophila [4].
• In addition, the AHR, ARNT, and SIM harbor a basic region helix-loop-helix motif in their N termini, whereas PER does not [8].
• Nasobemia (Ns) and spineless-aristapedia (ssa40a) are dominant and recessive homeotic mutants of Drosophila which convert parts of the antenna to leg structures [10].
• They also suggest that ds RNA3 is an intermediate in the synthesis of ss RNA3 [11].
• We provide genetic evidence that Dp(1;3)sta1 is mutant at the spineless (ss) locus and that it is associated with partial D-p40 activity [12].

Analytical, diagnostic and therapeutic context of ss

• In order to examine this issue, we developed an animal model that expresses the dioxin receptor homolog Spineless (Ss) ectopically in the Drosophila wing [7].

References