This behavior constitutes a cellular description of organ identity. elucidate the gene networks controlling and (for review, observe Han 1997); however, the mechanisms that take action downstream of these genes, to mediate pharyngeal organogenesis, are largely unknown. The genetic pathways that generate the ABa and MS cell lineages converge within the locus. Animals lacking zygotic activity fail to produce pharynx cells from either ABa or MS (Mango et al. 1994a). In addition, these mutants lack a rectum. The rectum is definitely descended from a third blastomere called ABp and does not derive from the pharyngeal cell lineages. Most other cells look like generated normally in mutant embryos, including cells from ABa and MS that are not part of the pharynx. Therefore, the locus is critical to generate a group of cells related by function (the digestive tract) rather than by cell lineage (ABa, MS) or cell type (pharynx neuron, pharynx muscle mass, etc.). This phenotype displays a transition during embryogenesis from maternal genes, like and that control entire cell lineages and broad domains of axial patterning, to zygotic genes, like that regulate the formation of specific organs, cells, and cell types. In the present study we address two potential mechanisms by which could function. First, could set up an organizing center that is critical for development of the entire pharynx. By analogy, loss of the anchor cell during vulval development results in no vulva becoming created (Greenwald 1997). Similarly, mutations in or c-lead to the absence of the kidney in mouse BNS-22 embryos (Kreidberg et al. 1993; Schuchardt et al. 1994). Each of these phenotypes displays a loss PROM1 in cell signaling. For vulval development, signaling happens between cells in two different organs, whereas in BNS-22 kidney formation and c-are necessary for epitheliomesenchymal relationships among different cells within the developing kidney primordium. A second possible explanation for function is that the protein could take action within individual pharyngeal cells to establish pharynx identity. That is, might be analogous to and the network of transcription factors that initiate vision formation (Desplan 1997). Loss-of-function mutations in either or prospects to a complete absence of the eye in Conversely, each of these BNS-22 genes, either only or in combination, is capable of inducing ectopic eyes. These phenotypes suggest that this group of factors synergize to define vision identity during development. In this statement we present evidence that encodes an homolog that is expressed in all pharyngeal precursors and establishes their fate. We suggest that and the eye genes symbolize a new class of developmental regulator that specifies organ identity. Given that genes have been implicated in gut development in other BNS-22 organisms (Kaufmann and Knochel 1996), we propose that specification of organ identity within the digestive tract may be a conserved feature of proteins. Results and Conversation pha-4 encodes the HNF-3 homolog Ce-fkh-1 and is indicated in the developing digestive tract To understand the molecular mechanism of function, we recognized the gene by a combination of positional cloning and candidate gene methods. Previous analyses showed that is located within the YAC Y79B4 (S. Mango, unpubl.). YAC Y79B4 contains the expected winged helix transcription element which was an excellent candidate to encode based on map position and mRNA manifestation (Azzaria et al. 1996; S. Mango, unpubl.). Three lines of evidence demonstrate that corresponds to First, extrachromosomal arrays transporting either the cosmid F38A6, which bears BNS-22 or a 16.7-kb PCR.