The pattern of adult sensilla in Drosophila is established by the dosage-sensitive interaction of two antagonistic groups of genes. Sensilla development is promoted by members of the achaete-scute complex and the daughterless gene whereas it is suppressed by whereas extramacrochaete

The pattern of sensilla of the adult Drosophila has been a recurrent theme in the study of pattern formation (OstenSacken, 1881; Sturtevant, 1921; Stern, 1968). A set of mechanoreceptors of the notum called macrochaeta or bristles has been particularly useful in these studies. Their conspicuous morphology and invariant position has greatly simplified the analysis of genetic variants and has allowed the identification of some gene activities involved in the construction of this pattern. The wild-type distribution of sensilla appears to be established by the activity of two groups of genes. The achaetescute gene complex (AS-C) and the daughterless (da) gene form the first group. Loss-of-function alleles of these loci prevent sensilla formation, whereas gain-of-function alleles of the AS-C elicit their ectopic appearance. This suggests that these genes are required for the specification of sensilla precursors (García-Bellido and Santamaría, 1978; García-Bellido, 1979; Dambly-Chaudière et al., 1988; García-Alonso and García-Bellido, 1986). The second group comprises extramacrochaetae (emc) and hairy (h). In contrast to the first group, loss-of-function alleles of emc and h induce the formation of ectopic sensilla, while a gain-of-function allele of emc causes loss of sensilla, suggesting that their activity antagonises that of the first group (Botas et al., 1982; García-Alonso and García-Bellido, 1988; Ingham et al., 1985; Ellis et al., 1990). In addition, alleles of the two groups of genes show characteristic dosage-sensitive interactions. For example, the extra bristles caused by emc and h are partially suppressed in an AS-C heterozygote and enhanced by an AS-C duplication (Moscoso del Prado and García-Bellido, 1984). These data suggest that the wild-type pattern of sensilla results from interactions amongst the two groups of genes. Other loci involved in sensilla patterning have been reported, the most notable being the neurogenic group. However, mutant alleles of these loci affect only the number of bristles generated at each position, rather than the position itself (see Shellenbarger and Mohler, 1978; Dietrich and Campos-Ortega, 1984; Simpson and Carteret, 1989; Hartenstein and Posakony, 1990; Mlodzik et al., 1990; Heitzler and Simpson, 1991 and reviews by Simpson, 1990a,b for further discussion) The products of these two groups of genes contain a conserved domain, term the Helix-Loop-Helix (HLH) motif (Villares and Cabrera, 1987; Alonso and Cabrera, 1988; Caudy et al., 1988; Rushlow et al., 1989; Ellis et al., 1990; Garrell and Modolell, 1990; Jarman et al., 1993). This domain contains two amphipathic helices connected by a flexible loop (FerréD’Amaré et al., 1993) as originally proposed by Murre et al. (1989b). HLH proteins can form both homodimers and heterodimers, mediated by hydrophobic contacts between the two 3595 Development 120, 3595-3603 (1994) Printed in Great Britain © The Company of Biologists Limited 1994