Tubes and the single C. elegans excretory cell.

The formation and regulation of tubule shape and size is fundamental to the development and function of many tissues and organs in metazoan organisms. The excretory canals of the nematode Caenorhabditis elegans are a fascinating example of cell morphogenesis, as the tiny worm manages to create a complicated set of tubular epithelia within a single cell. In addition to the inherent attraction of studying this cytoengineering feat, the excretory cell provides a simple genetically tractable model for studying tubule formation and regulation of tubule diameter. Mutations in the exc genes alter the diameter of the lumenal surface of these tubules. Cloning of these genes reveals a set of proteins that both control tubule diameter and regulate the comparative growth of the apical and basal tubular surfaces.

[1]  D. Hall,et al.  Cystic canal mutants in Caenorhabditis elegans are defective in the apical membrane domain of the renal (excretory) cell. , 1999, Developmental biology.

[2]  S. Brenner.  The genetics of Caenorhabditis elegans. , 1974, Genetics.

[3]  Park Ec,et al.  Mutations with dominant effects on the behavior and morphology of the nematode Caenorhabditis elegans. , 1986 .

[4]  D. Thierry-Mieg,et al.  Cloning by insertional mutagenesis of a cDNA encoding Caenorhabditis elegans kinesin heavy chain. , 1993, Proceedings of the National Academy of Sciences of the United States of America.

[5]  Douglas I. Johnson.  Cdc42: An Essential Rho-Type GTPase Controlling Eukaryotic Cell Polarity , 1999, Microbiology and Molecular Biology Reviews.

[6]  D. Riddle,et al.  Functional study of the Caenorhabditis elegans secretory-excretory system using laser microsurgery. , 1984, The Journal of experimental zoology.

[7]  V Praitis,et al.  sma-1 encodes a betaH-spectrin homolog required for Caenorhabditis elegans morphogenesis. , 1998, Development.

[8]  D. Hall,et al.  A putative GDP–GTP exchange factor is required for development of the excretory cell in Caenorhabditis elegans , 2001, EMBO reports.

[9]  W. Wadsworth,et al.  The C Domain of Netrin UNC-6 Silences Calcium/Calmodulin-Dependent Protein Kinase- and Diacylglycerol-Dependent Axon Branching in Caenorhabditis elegans , 2002, The Journal of Neuroscience.

[10]  J. Culotti,et al.  Multiple signaling mechanisms of the UNC-6/netrin receptors UNC-5 and UNC-40/DCC in vivo. , 2001, Genetics.

[11]  D. Moerman,et al.  UNC-52/perlecan isoform diversity and function in Caenorhabditis elegans. , 2001, Biochemical Society transactions.

[12]  S. Woodman,et al.  Microvascular Hyperpermeability in Caveolin-1 (−/−) Knock-out Mice , 2002, The Journal of Biological Chemistry.

[13]  B. Margolis,et al.  C. elegans cell migration gene mig-10 shares similarities with a family of SH2 domain proteins and acts cell nonautonomously in excretory canal development. , 1997, Developmental biology.

[14]  T. Pawson,et al.  UNC-73 Activates the Rac GTPase and Is Required for Cell and Growth Cone Migrations in C. elegans , 1998, Cell.

[15]  D. Hall,et al.  The unc-5, unc-6, and unc-40 genes guide circumferential migrations of pioneer axons and mesodermal cells on the epidermis in C. elegans , 1990, Neuron.

[16]  Y. Zheng,et al.  The Faciogenital Dysplasia Gene Product FGD1 Functions as a Cdc42Hs-specific Guanine-Nucleotide Exchange Factor* , 1996, The Journal of Biological Chemistry.

[17]  R. Hosono,et al.  Mutants of Caenorhabditis elegans with dumpy and rounded head phenotype , 1982 .

[18]  G. Walz,et al.  The Polycystic Kidney Disease 1 Gene Product Mediates Protein Kinase C α-dependent and c-Jun N-terminal Kinase-dependent Activation of the Transcription Factor AP-1* , 1998, The Journal of Biological Chemistry.

[19]  J. Vandekerckhove,et al.  unc-53 controls longitudinal migration in C. elegans. , 2002, Development.

[20]  A. Bretscher,et al.  Polarization of cell growth in yeast. I. Establishment and maintenance of polarity states. , 2000, Journal of cell science.

[21]  E. Hedgecock,et al.  Identification of epi-1 locus as a laminin alpha chain gene in the nematode Caenorhabditis elegans and characterization of epi-1 mutant alleles. , 1999, DNA sequence : the journal of DNA sequencing and mapping.

[22]  C. Kenyon,et al.  Characterization of beta pat-3 heterodimers, a family of essential integrin receptors in C. elegans , 1995, The Journal of cell biology.

[23]  David S. Park,et al.  Caveolin-1 mutations (P132L and null) and the pathogenesis of breast cancer: caveolin-1 (P132L) behaves in a dominant-negative manner and caveolin-1 (-/-) null mice show mammary epithelial cell hyperplasia. , 2002, The American journal of pathology.

[24]  D. Riddle.  C. Elegans II , 1998 .

[25]  J. Keene,et al.  Hel-N1: an autoimmune RNA-binding protein with specificity for 3' uridylate-rich untranslated regions of growth factor mRNAs. , 1993, Molecular and cellular biology.

[26]  R. Ellis,et al.  The Caenorhabditis elegans homolog of FGD1, the human Cdc42 GEF gene responsible for faciogenital dysplasia, is critical for excretory cell morphogenesis. , 2001, Human molecular genetics.

[27]  David S. Park,et al.  Caveolin-1-deficient Mice Are Lean, Resistant to Diet-induced Obesity, and Show Hypertriglyceridemia with Adipocyte Abnormalities* , 2002, The Journal of Biological Chemistry.

[28]  K. Roepstorff,et al.  Caveolae are highly immobile plasma membrane microdomains, which are not involved in constitutive endocytic trafficking. , 2002, Molecular biology of the cell.

[29]  G. Garriga,et al.  Genes necessary for C. elegans cell and growth cone migrations. , 1997, Development.

[30]  G. Ruvkun,et al.  Regulation of ectodermal and excretory function by the C. elegans POU homeobox gene ceh-6. , 2001, Development.

[31]  H. Hutter,et al.  Conservation and novelty in the evolution of cell adhesion and extracellular matrix genes. , 2000, Science.

[32]  T. Kawano,et al.  Neuronal expression of a Caenorhabditis elegans elav-like gene and the effect of its ectopic expression. , 1999, Biochemical and biophysical research communications.

[33]  M. Bundgaard,et al.  The three-dimensional organization of plasmalemmal vesicular profiles in the endothelium of rat heart capillaries. , 1983, Microvascular research.

[34]  J. Rossen,et al.  The MUC family: an obituary. , 2002, Trends in biochemical sciences.

[35]  J. Ahringer,et al.  CDC-42 controls early cell polarity and spindle orientation in C. elegans , 2001, Current Biology.

[36]  W. Almers,et al.  Imaging actin and dynamin recruitment during invagination of single clathrin-coated pits , 2002, Nature Cell Biology.

[37]  D. Hall,et al.  Genetics of cell and axon migrations in Caenorhabditis elegans. , 1987, Development.

[38]  D. Drubin,et al.  Origins of Cell Polarity , 1996, Cell.

[39]  A. Otsuka,et al.  The C. elegans unc-104 4 gene encodes a putative kinesin heavy chain-like protein , 1991, Neuron.

[40]  G. Garriga,et al.  Neuronal Migrations and Axon Fasciculation Are Disrupted in ina-1 Integrin Mutants , 1997, Neuron.

[41]  C. Hunter,et al.  CDC-42 regulates PAR protein localization and function to control cellular and embryonic polarity in C. elegans , 2001, Current Biology.

[42]  A. Bretscher,et al.  Polarization of cell growth in yeast. , 2000, Journal of cell science.

[43]  I. Nabi,et al.  Caveolin-1 Is a Negative Regulator of Caveolae-mediated Endocytosis to the Endoplasmic Reticulum* , 2002, The Journal of Biological Chemistry.

[44]  F. Sotgia,et al.  Impairment of caveolae formation and T-system disorganization in human muscular dystrophy with caveolin-3 deficiency. , 2002, The American journal of pathology.

[45]  M. Labouesse,et al.  A Conserved Interaction between β1 Integrin/PAT-3 and Nck-Interacting Kinase/MIG-15 that Mediates Commissural Axon Navigation in C. elegans , 2002, Current Biology.

[46]  R. D. Rudic,et al.  In vivo delivery of the caveolin-1 scaffolding domain inhibits nitric oxide synthesis and reduces inflammation , 2000, Nature Medicine.

[47]  T. Oka,et al.  Four subunit a isoforms of Caenorhabditis elegans vacuolar H+-ATPase. Cell-specific expression during development. , 2001, The Journal of biological chemistry.

[48]  Cell and Growth Cone Migrations , 1997 .

[49]  J. A. Steitz,et al.  HuR and mRNA stability , 2001, Cellular and Molecular Life Sciences CMLS.

[50]  P. Strålfors,et al.  Cholesterol Depletion Disrupts Caveolae and Insulin Receptor Signaling for Metabolic Control via Insulin Receptor Substrate-1, but Not for Mitogen-activated Protein Kinase Control* , 2001, The Journal of Biological Chemistry.

[51]  G. Christ,et al.  Caveolin-2-Deficient Mice Show Evidence of Severe Pulmonary Dysfunction without Disruption of Caveolae , 2002, Molecular and Cellular Biology.

[52]  W. Möbius,et al.  Intracellular Distribution of a Biotin-labeled Ganglioside, GM1, by Immunoelectron Microscopy After Endocytosis in Fibroblasts , 1999, The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society.

[53]  J. Sulston,et al.  The embryonic cell lineage of the nematode Caenorhabditis elegans. , 1983, Developmental biology.

[54]  H. Horvitz,et al.  The Caenorhabditis elegans gene lin-17, which is required for certain asymmetric cell divisions, encodes a putative seven-transmembrane protein similar to the Drosophila frizzled protein. , 1996, Genes & development.

[55]  P. Oh,et al.  Dynamin at the Neck of Caveolae Mediates Their Budding to Form Transport Vesicles by GTP-driven Fission from the Plasma Membrane of Endothelium , 1998, The Journal of cell biology.

[56]  M. Lisanti,et al.  Co-purification and Direct Interaction of Ras with Caveolin, an Integral Membrane Protein of Caveolae Microdomains , 1996, The Journal of Biological Chemistry.