Mains PE (1994) Worm Breeder's Gazette "Interactions Between mei-1 and the unc-116 Kinesin"

Mains PE

[Worm Breeder's Gazette, 1994]

Interactions Between mei-l and the unc-116 Kinesin Paul E. Mains, Dept. of Medical Biochemistry, University of Calgary, Calgary, Alberta, Canada

Wissmann AK et al. (1994) Worm Breeder's Gazette "Characterization of the let-502 Gene"

Mains PE, Wissmann AK, McGhee JD

[Worm Breeder's Gazette, 1994]

Characterization of the let-502 gene Andreas Wissmann, James D. McGhee and Paul E. Mains, Dept. of Medical Biochemistry, University of Calgary, Calgary, Alberta, Canada T2N 4N1

Dhillon HS et al. (1994) Worm Breeder's Gazette "More Degenerins in the Worm?"

Dhillon HS, Driscoll MA

[Worm Breeder's Gazette, 1994]

More degenerins in the worm? Harbinder Singh Dhillon and Monica Driscoll. Department of Molecular Biology and Biochemistry, Rutgers University, Center for Advanced Biotechnology and Medicine, 679 Hoes lane, Piscataway, N.J. 08855

Sommer RJ et al. (1994) Worm Breeder's Gazette "Evolution of Vulva-Formation: Part II: Species With a Central Vulva"

Sommer RJ, Sternberg PW

[Worm Breeder's Gazette, 1994]

Evolution of vulva-formation: Part II: Species with a central vulva Ralf J. Sommer & Paul W. Sternberg, California Institute of Technology, Division of Biology 156-29, Pasadena, CA 91125

Li WQ et al. (1992) Worm Breeder's Gazette "Characterization of the Axonal Guidance and Outgrowth gene Unc-33"

Shaw JE, Li WQ, Herman RK

[Worm Breeder's Gazette, 1992]

Characterization of the axonal guidance and outgrowth gene unc-33 W. Li, R. K. Herman and J. E. Shaw Department of Genetics and Cell biology, University of Minnesota, St Paul, MN 55108

Sommer RJ et al. (1994) Worm Breeder's Gazette "Evolution of Vulva Formation: Part IV: Variation in AC Position Can Cause a Shift of Vulva Formation Towards P(4-6).p."

Sternberg PW, Sommer RJ

[Worm Breeder's Gazette, 1994]

Evolution of vulva formation: Part IV: Variation in AC position can cause a shift of vulva formation towards p(4- 6).p Ralf J. Sommer & Paul W. Sternberg, HHMI & California Institute of Technology, Division of Biology 156-29, Pasadena, CA

Hall DH et al. (1994) Worm Breeder's Gazette "Cytology of Degenerin-Induced Cell Death in the PVM Neuron"

Driscoll MA, Chalfie M, Gu GQ, Hall DH, Gong L

[Worm Breeder's Gazette, 1994]

Cytology of degenerin-induced cell death in the PVM neuron David H. Hall, Guoqiang Gu+, Lei Gong#, Monica Driscoll#, and Martin Chalfie+, * Dept. Neuroscience, Albert Einstein College of Medicine, Bronx, N.Y. 10461 + Dept. Biological Sciences, Columbia University, New York, N.Y. 10027 # Dept. Molecular Biology and Biochemistry, Rutgers University, Piscataway, N.J. 08855

Johnson, Christina K. et al. (2021) MicroPubl Biol

Miller, David D., Johnson, Christina K., Bianchi, Laura

[MicroPubl Biol, 2021]

MEC-4 and UNC-8 are subunits of the DEG/ENaC family of voltage-independent Na+ channels in C. elegans (Driscoll and Chalfie 1991, Canessa, Horisberger et al. 1993, Waldmann, Champigny et al. 1996, Waldmann, Champigny et al. 1997, de Weille, Bassilana et al. 1998, Waldmann and Lazdunski 1998). While MEC-4 is expressed in body touch neurons where it mediates the transduction of gentle touch sensation (Driscoll and Chalfie 1991, O'Hagan, Chalfie et al. 2005), UNC-8 is primarily expressed in motoneurons where it is involved in synaptic remodeling during development (Tavernarakis, Shreffler et al. 1997, Miller-Fleming, Petersen et al. 2016). Both MEC-4 and UNC-8 can be hyperactivated by genetic mutations that hinder channel closing, called (d) mutations (Driscoll and Chalfie 1991, Shreffler, Magardino et al. 1995, Goodman, Ernstrom et al. 2002, Wang, Matthewman et al. 2013). C. elegans neurons and Xenopus oocytes expressing these hyperactive variants of MEC-4 and UNC-8 undergo cell death due to uncontrolled flux of ions into the cell. Cell death in Xenopus oocytes and in cultured C. elegans neurons can be prevented by incubation with the DEG/ENaC channel blocker amiloride (Goodman, Ernstrom et al. 2002, Suzuki, Kerr et al. 2003, Wang, Matthewman et al. 2013).

Driscoll MA et al. (1991) Nature "The mec-4 gene is a member of a family of Caenorhabditis elegans genes that can mutate to induce neuronal degeneration."

Driscoll MA, Chalfie M

[Nature, 1991]

Three dominant mutations of mec-4, a gene needed for mechanosensation, cause the touch-receptor neurons of Caenorhabditis elegans to degenerate. With deg-1, another C. elegans gene that can mutate to induce neuronal degeneration and that is similar in sequence, mec-4 defines a new gene family. Cross-hybridizing sequences are detectable in other species, raising the possibility that degenerative conditions in other organisms may be caused by mutations in similar genes. All three dominant mec-4 mutations affect the same amino acid. Effects of amino-acid substitutions at this position suggest that steric hindrance may induce the degenerative state.AD - Department of Biological Sciences, Columbia University, New York, New York 10027.FAU - Driscoll, MAU - Driscoll MFAU - Chalfie, MAU - Chalfie MLA - engSI - GENBANK/M31718SI - GENBANK/X52371SI - GENBANK/X52372SI - GENBANK/X56198SI - GENBANK/X56199SI - GENBANK/X57181SI - GENBANK/X57182SI - GENBANK/X57183SI - GENBANK/X57184SI - GENBANK/X58982PT - Journal ArticleCY - ENGLANDTA - NatureJID - 0410462SB - IMSB - S

Dhaval S Patel et al. (2003) International Worm Meeting "Modelling Multiplicity: A Comparative Model of the C. elegans DAF-2 Receptor Tyrosine Kinase."

Manoj Nanji, David Gems, Acely Garza, Paul C Driscoll, Dhaval S Patel

[International Worm Meeting, 2003]

The DAF-2 insulin/IGF-1-like receptor is a key regulator of development and ageing. Characterisation of temperature-sensitive hypomorphic alleles of daf-2 has revealed two overlapping pleiotropic classes. Class 1 alleles display constitutive dauer larva formation, increased thermotolerance and increased longevity. The class 2 alleles also display these traits, plus others including reduced adult motility, reduced brood size, early larval arrest and embryonic lethality. The vertebrate insulin and IGF-1 receptors have been shown to activate several different signalling pathways. The DAF-2 receptor has so far only been shown to regulate a conserved PI3K pathway that acts to inhibit DAF-16, a FOXO transcription factor homologue. Yet the C. elegans genome contains many predicted genes that are putative homologues of proteins known to interact with insulin/IGF-1 receptors in vertebrates, such as Shc, Grb2 and IIP-1. The presence of such homologues suggests that DAF-2 may interact with multiple signalling pathways. Moreover, genes encoding at least 39 putative insulin-like ligands have been identified, suggesting the existence of different modes of DAF-2 activation/ inhibition. To gain a better understanding of DAF-2 function we have used a combination of sequence and phenotypic data for 18 different daf-2 alleles, epistasis analysis and comparative homology-based modelling, using structural data for the IGF-1 receptor, to develop a structure-function model of the DAF-2 receptor.