Identification of C. elegans sensory ray genes using whole-genome expression profiling

• Published in: Developmental biology 2004-06, Vol.270 (2), p.499-512
• Main Authors: Portman, Douglas S, Emmons, Scott W
• Format: Article
• Language: English
• Subjects: Animals; C. elegans; Caenorhabditis elegans; Caenorhabditis elegans - embryology; Caenorhabditis elegans - genetics; Caenorhabditis elegans Proteins - genetics; Caenorhabditis elegans Proteins - metabolism; Cell Differentiation - physiology; Databases, Genetic; DNA microarrays; E-Box Elements - genetics; Gene Expression Profiling; Genes, Reporter - genetics; Genetic network; lin-32; Male; Male tail; Neural subtype; Oligonucleotide Array Sequence Analysis; Polycystins; Proneural; Sensory rays; Sensory Receptor Cells - cytology; Sensory Receptor Cells - embryology; Transcription Factors - genetics; Transcription Factors - metabolism
• ISSN: 0012-1606; 1095-564X
• DOI: 10.1016/j.ydbio.2004.02.020

The three cells that comprise each C. elegans sensory ray (two sensory neurons and a structural cell) descend from a single neuroblast precursor cell. The atonal ortholog lin-32 and the E/ daughterless ortholog hlh-2 act to confer neural competence during ray development, but additional regulatory factors that control specific aspects of cell fate are largely unknown. Here, we use full-genome DNA microarrays to compare gene expression profiles in adult males of two mutant strains to identify new components of the regulatory network that controls ray development and function. This approach identified a large set of candidate ray genes. Using reporter genes, we confirmed ray expression for 13 of these, including a β-tubulin, a TWK-family channel, a putative chemoreceptor and four novel genes (the cwp genes) with a potential role in sensory signaling through the C. elegans polycystins lov-1 and pkd-2. Additionally, we have found several ray-expressed transcription factors, including the Zn-finger factor egl-46 and the bHLH gene hlh-10. The expression of many of these genes requires lin-32 function, though this requirement may not reflect direct activation by lin-32. Our strategy provides a complementary foundation for modeling the genetic network that controls the development of a simple sensory organ.