C. elegans peb-1 mutants exhibit pleiotropic defects in molting, feeding, and morphology

• Published in: Developmental biology 2004-12, Vol.276 (2), p.352-366
• Main Authors: Fernandez, Anthony P., Gibbons, Jack, Okkema, Peter G.
• Format: Article
• Language: English
• Subjects: Animals; Caenorhabditis elegans - anatomy & histology; Caenorhabditis elegans - growth & development; Caenorhabditis elegans - physiology; Caenorhabditis elegans Proteins - genetics; Caenorhabditis elegans Proteins - metabolism; Cell Differentiation; Digestive System - anatomy & histology; Digestive System - metabolism; DNA-binding protein; DNA-Binding Proteins - genetics; DNA-Binding Proteins - metabolism; Feeding Behavior; FLYWCH motif; g1 gland cell; Gene Expression Regulation, Developmental; Genes, Reporter; Hindgut; Hypodermis; Larva - anatomy & histology; Larva - physiology; Larva - ultrastructure; Microscopy, Video; Molting - genetics; Molting defective; peb-1; Pharynx; Phenotype; Recombinant Fusion Proteins - genetics; Recombinant Fusion Proteins - metabolism; Trans-Activators - genetics; Trans-Activators - metabolism; Transgenes
• ISSN: 0012-1606; 1095-564X
• DOI: 10.1016/j.ydbio.2004.08.040

Caenorhabditis elegans PEB-1 is a novel DNA-binding protein expressed in most pharyngeal cell types and outside the pharynx in the hypodermis, hindgut, and vulva. Previous RNAi analyses indicated that PEB-1 is required for normal morphology of these tissues and growth; however, the peb-1 null phenotype was unknown. Here we describe the deletion mutant peb-1(cu9) that not only exhibits the morphological defects observed in peb-1(RNAi) animals, but also results in penetrant larval lethality characterized by defects in pharyngeal function and molting. Consistent with a function in molting, we found that PEB-1 was detectable in all hypodermal and hindgut cells underlying the cuticle. Comparison to molting-defective lrp-1(ku156) mutants revealed that the peb-1(cu9) mutants were particularly defective in shedding the pharyngeal cuticle, and this defect likely contributed to feeding defects and lethality. Most markers of pharyngeal cell differentiation examined were expressed normally in peb-1(cu9) mutants; however, g1 gland cell expression of a kel-1∷gfp reporter was reduced. As g1 gland cells have prominent functions during molting, we suggest defective gland cell differentiation contributes to peb-1(cu9) molting defects. In comparison, other peb-1 mutant phenotypes, including hindgut abnormalities, appeared independent of the molting defect. Similar phenotypes resulted from late loss of pha-4 function, suggesting that PEB-1 and PHA-4 have common functions in some tissues where they are co-expressed.