Gene Dmel\ct

ct mutations fall into three nonoverlapping phenotypic classes: kinked femur, cut wings, and lethal. Kinked- femur mutants are small with slightly dark, dull, red eye color; femurs kinked; wings seldom expand following eclosion, or when they do expand they are opaque and abnormal in shape; flies seem unable to move normally and die on the food soon after eclosion. Cut-wing mutants variably affect wing shape and head capsule development; phenotypic effects include incised wing margins with the tips usually cut to points, missing or ventrally displaced vibrissae, deformed antennae, e.g., flattened and embedded with aristae concave forward, smaller kidney-shaped eyes, warped abdominal bands, and fine bristles. Most lethal alleles survive as clones of homozygous epidermal cells (Demerec). Developmental study of ct6 by Waddington [1939, Proc. Nat. Acad. Sci. USA 25: 299-308; 1940, J. Genet. 41: 75-139 (fig.)] shows wing bud narrower than wild type as early as just after eversion of wing in early pupa. Cell death observed in prepupal wing bud (D. Fristrom, 1969, Mol. Gen. Genet. 103: 363-79). Clones of ct6 cells in internal areas of wing blade normal in size; marginal clones much reduced in size indicating cell death. Homozygous clones in either dorsal or ventral membrane must reach margin in order to produce incision, 100/127 marginal clones unassociated with gaps; when gaps are produced, they affect both wing surfaces even though clone confined to a single surface. Both dorsal and ventral chaetal elements at the edges of such gaps may show the markers of such clones (Santamaria and Garc'a-Bellido, 1975, Wilhelm Roux's Arch. Entwicklungsmech. Org. 178: 233-45). Lethal alleles fall into three groups, based on their complementation characteristics: cutless, group I, and group II. Lethal alleles ctC145, ctJA124, and ctl49 exhibit polyphasic lethality from late embryo to pharate adult (Johnson and Judd, 1979). Lethal embryos characterized by posterior defects in spiracles; no Keilin's organs, and abnormal maxillary complex (Wieschaus, Nusslein-Volhard, and Jurgens, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 296-307). Group II and to a slightly lesser degree group I lethals fail to differentiate external sensory neurons in the peripheral nervous system; the presumptive external sensory neurons of the embryonic peripheral nervous system and their support cells are transformed into chordotonal neurons with their support cells; the transformed organs are chordotonal both in morphology and antigenic specificity. Same effect seen in the adult sensory organs in mosaics; embryonic effect differs from that seen in adults in that embryos lack peripheral sensory structures, e.g., Keilin's organs, whereas such structures persist, though reduced in size, in adult tissue. The numbers and positions of peripheral neurons is normal. CNS structure and function appear normal. No discernable effect of absence of ct function in the maternal germ line. Effect of ct mutations on PNS differentiation cell autonomous. [Bodmer, Barbel, Sheperd, Jack, Jan, and Jan, 1987, Cell 51: 293-307 (fig.).] Antibodies to ct protein specifically bind to nuclei of presumptive external sensory organ cells including those of the antennamaxillary organ and external sensory organs in spiracles, but not to nuclei of chordotonal organs; antibody staining also seen in some neurons with multiple dendritic arborizations and in cells lining the Malpighian tubules (Blochlinger, Bodmer, Jack, Jan, and Jan, 1988, Nature 333: 629-35). Kinked-femur, cut-wing, and cutless alleles are mutually complementing: group I lethals complement kinked-femur but not cut-wing alleles; and group II lethals are noncomplementing; all combinations of lethal alleles are lethal. The different phenotypic classes of alleles occupy discrete and separate regions of the complex, with the order from left to right being, kinked femur, cut wing, group I lethals, and group II lethals; cutless alleles have not been mapped. Kinked femur, cut, and group-I-lethal mutations are associated with chromosome aberrations or insertions of transposable elements, whereas group II lethals appear to be point mutations. ct6, ct68E (= ct67s?), ct78a, and ctK suppressed by su(Hw)2; dvr2 enhances ct6 and inhibits its complete suppression by su(Hw)2; su(Hw)2/+ shows slight dominant suppression of wing phenotype of ctK (Lee, 1973, Aust. J. Biol. Sci. 26: 903-09). ct6 and ctK strongly enhanced by su(s); su(s) ctK lethal (Johnson) but rescued by su(Hw)2/+ (Craymer). ct6 the most commonly used allele.

           
                                                               ct
kf2   ctnct6                           ctK                lethals
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|       | |                             |                       |
|  -0.04- |           -0.16-            |     - ~0.07-          |
         Genetic fine structure map of the cut locus

           

Classified as a group-I lethal because homozygotes show reduced viability, and only 10% of fewer heterozygotes with other lethal alleles survive; survivors have weakly cut wings, as well as fine bristles, and enlarged and deformed humeral callus, not seen in other cut-wing mutants.

Acts as a lethal allele in combination with deficiencies for ct; phenotype normal in combination with viable ct alleles. Homozygotes have reduced viability and show thoracic protuberances (Schalet). Heterozygotes of ctcl with lethal alleles of ct die or eclose in small numbers; an exception is ctcl/ctHA46, which exhibits normal survival.

Lethal; a member of cut Lethal II group, maps proximal to ctC145 (Jack, 1985). Not suppressed by su(Hw)2 (Schalet). ctlS1/+ males, frequently show thoracic protuberances (Schalet).

Almost complete lethal; survival less than 1%. Not suppressed by su(Hw)2; cut-cutless type of mutant in that ctlS2 fails to complement lethal alleles, e.g. ctlS1, but complements kf2, ct6 and ctS. Rare surviving males and females are fertile with normal wings, but usually show thoracic protuberances in the region of the presutural and notoplural bristles as are also seen in heterozygotes of ctlS1, Df(1)ctJ4 or Df(1)ctJ6.