Gene Dmel\Dl

A haplo-insufficient member of the group of neurogenic genes originally described on the basis of its dominant phenotype. Several classes of alleles designated by Vassin and Campos-Ortega based on the phenotype of heterozygous adults: Amorphic and strong hypomorphic alleles display wing veins widened at their junctions with the margin to form delta-like structures; in addition, they show irregular thickening of vein 2, and wings frequently held in divergent attitude; fusion of ommatidia may give rise to disruptions in regular hexagonal array of eye facets; ocelli are slightly enlarged; additional bristles are present on head, thorax, and abdomen; homozygotes die as embryos. Rare antimorphic alleles display the above phenotype in exaggerated form with irregular widening of all longitudinal wing veins, enlarged deltas, regularly divergent wings, smaller rougher eyes, larger and often fused ocelli, and further increase in the numbers of extra bristles; in addition, tarsal joints 2 to 4, but not 5 are fused; homozygotes are embryonic lethals. Rare recessive alleles show low levels of survival as homozygotes or trans heterozygtoes with more severe alleles; survivors usually display a less extreme version of the phenotype exhibited by heterozygotes for amorphic alleles; however, some combinations are wild type in appearance and others (e.g., the antimorphs) are lethal. The embryonic lethality of homozygotes displays the typical neurogenic phenotype with neural hyperplasia accompanied by epidermal aplasia; most or all cells of the neurogenic ectoderm recruited into the neurogenic pathway. Transplantation of homozygous Dl pole cells demonstrate Dl expression during oogenesis (Dietrich and Campos-Ortega, 1984, J. Neurogenet. 1: 315-32). Dl classed as non-autonomous in that single cells from the neurogenic ectoderm of Dl- embryos are capable of giving rise to both neural and epidermal derivatives when transplanted into the neurogenic region of wild-type embryos, suggesting that Dl- cells are capable of responding normally to information from neighboring cells (Technau and Campos-Ortega, 1987, Proc. Nat. Acad. Sci. USA 84: 4500-04). Transcription in cellular blastoderm seen in the ventrolateral neurogenic ectoderm, with a ventral-to-dorsal gradient of expression, corresponding to the gradient of neurogenic capabilities of the neurogenic ectoderm. During gastrulation a metameric pattern of expression appears, disappears, and reappears; as development proceeds complicated spatial and temporal specificities of expression ensue (Vassin et al., 1987). Interactions with other neurogenic mutations complex; Dl mutations suppress the spl-enhancing effect of E(spl) (Shepard, Boverman, and Muskavitch, 1988, Genetics 122: 429-38) and the expression of Ax (Siren and Portin, 1989, Genet. Res. 54: 23-26); severe alleles fail to survive in heterozygotes with E(spl) loss-of-function alleles [Lehmann, Dietrich, Jimenez, and Campos-Ortega, 1981, Wilhelm Roux's Arch. Dev. Biol. 190: 226-29 (fig.)] especially when E(spl) is maternally inherited. Expression of Dl/+ observed to be partially suppressed by duplications for E(spl)+ (Vassin, Vielmetter, and Campos-Ortega, 1985, J. Neurogenet. 2: 291-308), yet, de la Concha, Dietrich, Weigel, and Campos-Ortega (1988, Genetics 118: 499-508) report that extra doses of E(spl)+ enhance the neurogenic phenotype of Dl-. Dl/+ and Dl- phenotypes are suppressed by heterozygous and homozygous deficiencies for H, respectively. For example, H2 is able to suppress the phenotypic effects of Dl9P, either in Dl9P/+ or in Dl9P/Dl9P genotypes; Dl9P/Dl9P is cell lethal in both the eye and the cuticle; Dl9P H2/Dl9P H2 cells, on the other hand, develop nearly normally (Dietrich and Campos-Ortega, 1984). Expression of Dl enhanced by duplications for N+ or H+, and three doses of Dl+ enhance expression of N- and neu-, but reduce the severity of the mam- phenotype. de la Concha, et al. have incorporated many of these observations into a model of neurogenic-gene interaction. Dl alleles interact synergistically with certain Minutes, producing extreme phenotypes and drastically lowered viability (Schultz, 1929, Genetics 14: 366-419); DlOf enhances spaCat (Tsukamoto, 1956, DIS 30: 79).

Like Dl1 except that severity of phenotype in homozygous embryos temperature sensitive. At 18 there is patchy neuralization of cephalic and ventral ectoderm; expression more severe at 25 and extreme at 29. Temperature-sensitive period between pole-cell formation and mesodermal segmentation. Clone of ommatidia homozygous for Dl6B, normal when reared under permissive conditions; in flies raised at 29C, however, ommatidial pattern severely disturbed, producing scarring of the eye surface; ommatidia appear larger than normal and interommatidial bristles missing; homozygous mutant facets contain more than a normal complement of retinula cells-up to 13; cytodifferentiation apparently normal. Cuticular clones exhibit elaboration of extra bristles at bristle-forming sites [Dietrich and Campos-Ortega, 1984, J. Neurogenet. 1: 315-32 (fig.)].

The most severe antimorphic allele (Vassin and Campos-Ortega, 1987). All components of the phenotype of heterozygosity for a Dl deletion are present in a drastically increased manner in heterozygotes for DlB107 (or for DlFE30 or DlFE32). All wing veins are irregularly widened, veins 3 and 5 being broadened along their whole lengths (same for vein 2 in DlFE30 and DlFE32) and are occasionally incised posteriorly; the deltas formed at the wing margins are larger and the wings are held spread with complete penetrance. The eyes are smaller and rougher. There is also a severe disturbance of the normal bristle pattern on the head, thorax, and abdomen owing to a further increase in the number of bristles. The ocelli are larger and often fused together, thus forming a half circle. Finally, tarsal segments 2 to 4 are fused, but segment 5 is never found to be affected.

Three alleles survive as homozygotes (Vassin, and Campos-Ortega, 1987). Slight delta-like thickenings at posterior tips of wing veins 2, 3, 4 and 5; roughening of eye. Dlvi homozygotes also show shortening and frequent fusion of tarsal segments. A few homozygous embryos fail to hatch, showing patchy neuralization in cephalic and ventral territories. Dlvi/+ normal. Trans heterozygotes with dominant alleles show extreme wing, eye, and tarsal abnormalities; Dlvi1 lethal in combination with DlF30, DlF32 DlE50-2, and DlB107 (Vassin, and Campos-Ortega, 1987).