Genetic evidence suggests that E(spl), one of the neurogenic loci of Drosophila, is a gene complex comprising an as yet incompletely established number of transcription units. In order to correlate the various transcription units with E(spl) functions, wild‐type flies were transformed with genomic DNA encoding the transcription unit m8 from the mutant E(spl)D, which was known to be altered in embryos carrying this mutant allele. Transformants show the same dominant enhancement of the spl phenotype as E(spl)D itself. Since m8 has a virtually identical pattern of expression as m4, m5 and m7, we have determined the sequence of these four transcripts. The deduced protein products of m5, m7 and m8 exhibit extensive sequence homology with each other. All three encode a sequence similar to one of the conserved domains of representatives of the vertebrate myc gene family which is also present in the deduced protein sequences of the Drosophila achaete‐scute gene complex. Sequence analysis of the m8 transcription unit in the E(spl)D mutation revealed several DNA lesions. One of the lesions is a deletion in the region upstream of the transcription start site. Another lesion is a deletion in the coding region that leads to a shorter protein which, in addition, differs in its carboxy‐terminal end from the wild‐type protein by the presence of nine amino acids.

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Enhancer of split [E(spl)], one of the neurogenic loci of Drosophila, is located in bands 96F8‐13. One hundred and fifty kilobases of genomic DNA, spanning the E(spl) locus, were cloned by chromosomal walking. DNA heterogeneities associated with eleven E(spl) mutations, including three Pr alleles, were mapped to a region of 36 kb, and an additional one outside of this region. One of these mutations is a deletion of ˜34 kb that causes severe neural hyperplasia of homozygous embryos with complete penetrance. Mutations associated with DNA polymorphisms mapping within smaller regions do not lead to a fully penetrant neurogenic phenotype. The 36‐kb region encodes 11 major transcripts, which exhibit distinct temporal and/or spatial patterns of expression. The expression of one of these transcripts is modified in two different mutants. In addition, one of the mutants [E(spl)D] shows another transcript, which is not present in the wild‐type and co‐exists with the remaining transcripts. We suggest that more than one of the 11 transcripts are necessary for a normal function of the E(spl) locus. The spatial distribution of four of these RNAs, which exhibit almost identical patterns of expression, strongly suggests that the encoded proteins are required for the process of segregation of neural and epidermal lineages.

How cells coordinate their spatial positioning through intercellular signaling events is poorly understood. Here we address this topic using Caenorhabditis elegans vulval patterning during which hypodermal vulval precursor cells (VPCs) adopt distinct cell fates determined by their relative positions to the gonadal anchor cell (AC). LIN-3/EGF signaling by the AC induces the central VPC, P6.p, to adopt a 1° vulval fate. Exact alignment of AC and VPCs is thus critical for correct fate patterning, yet, as we show here, the initial AC-VPC positioning is both highly variable and asymmetric among individuals, with AC and P6.p only becoming aligned at the early L3 stage. Cell ablations and mutant analysis indicate that VPCs, most prominently 1° cells, move towards the AC. We identify AC-released LIN-3/EGF as a major attractive signal, which therefore plays a dual role in vulval patterning (cell alignment and fate induction). Additionally, compromising Wnt pathway components also induces AC-VPC alignment errors, with loss of posterior Wnt signaling increasing stochastic vulval centering on P5.p. Our results illustrate how intercellular signaling reduces initial spatial variability in cell positioning to generate reproducible interactions across tissues.