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"

McGhee JD, Wissmann AK, Mains PE

[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

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

Sternberg PW, Sommer RJ

[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"

Herman RK, Shaw JE, Li WQ

[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

Simske JS et al. (1994) Worm Breeder's Gazette "Specification of Vulval Cell Fates By Sequential Signalling Pathways."

Kim SK, Simske JS

[Worm Breeder's Gazette, 1994]

Specification of vulval cell fates by sequential signaling pathways Jeffrey S. Simske and Stuart K. Kim, Dept. of Developmental Biology, Stanford University Medical Center, Stanford CA 94305

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

Roque CG et al. (2018) Neuron "Wimpy Nerves: piRNA Pathway Curbs Axon Regrowth after Injury."

Hengst U, Roque CG

[Neuron, 2018]

While PIWI-interacting RNAs (piRNAs) are primarily recognized as guardians of genome integrity, new functions of these small non-coding RNAs are emerging. In this issue, Kim etal. (2018) describe a piRNA-based mechanism that limits axon regeneration in C.elegans.

Irazoqui JE (2014) Cell Host Microbe "DAF-tly depart stinky situations with elegans."

Irazoqui JE

[Cell Host Microbe, 2014]

During acute infection our behavior tends to change. Despite how common sickness behavior is, its molecular basis is not well understood. In a study published in Cell, Kim and colleagues (Meisel etal., 2014) implicate bacterial secondary metabolites as triggers of neural TGF-? signaling, which results in behavioral change during infection.

Vader G et al. (2014) Dev Cell "HORMA domains at the heart of meiotic chromosome dynamics."

Vader G, Musacchio A

[Dev Cell, 2014]

HORMA domain proteins are required for the careful orchestration of chromosomal organization during meiosis. Kim et al. (2014) and Silva et al. (2014) now provide structural and functional insights into the roles of C. elegans HORMA proteins, revealing parallels to the function of the HORMA protein MAD2 in mitotic checkpoint signaling.

Lucinda Carnell et al. (2003) International Worm Meeting "Amphetamine, Dopamine, and Behavior of C. elegans"

Lucinda Carnell, Steven McIntire, Paul Kim, Swung Woo Hong, Julie Illi

[International Worm Meeting, 2003]

Amphetamine, as well as other psychostimulants such as cocaine and methylphenidate, has a high potential for abuse. The primary mechanism of action of these drugs is the inhibition of the dopamine plasma membrane transporter (DAT) which results in elevated levels of dopamine at the synapse. These drugs can cause long lasting synaptic changes upon repeated exposure that may be important for their subsequent addictive properties. We are interested in characterizing the mechanisms that contribute to amphetamine modulation of dopaminergic pathways.Administration of amphetamine to wild-type animals results in a dose dependent inhibition of locomotion, egg laying, and pharyngeal pumping. These behavioral effects are similar to those produced by exposing animals to exogenous dopamine, suggesting that amphetamine may act on dopaminergic pathways in C. elegans. We completed a genetic screen of 5200 genomes to identify mutants resistant to the effects of amphetamine on locomotion and identified eight candidates. We then characterized the mutants for defects in a specific dopamine-mediated behavior previously described by Sawin et al (Neuron 26: 619-31, 2000). Sawin demonstrated that mutants defective in the synthesis of dopamine fail to slow upon re-entry onto a bacterial lawn. Four of the amphetamine resistant mutants show an absence of slowing or reduced slowing in this assay. None of the mutants showed other obvious phenotypes. To distinguish between possible pre- and postsynaptic defects at dopaminergic synapses, we tested these mutants for resistance to exogenous dopamine. All of these mutants proved sensitive to exogenous dopamine suggesting presynaptic defects or abnormalities upstream of the dopaminergic synapses. In order to find mutants resistant to the effects psychostimulants due to postsynaptic defects, we initiated a genetic screen for animals resistant to the inhibitory effect of exogenous dopamine on thrashing in liquid. In a screen of 2500 genomes, we identified three mutants (eg643, eg644 and eg645) resistant to the effects of exogenous dopamine. Additional pharmacological experiments revealed altered sensitivity of some of these mutants to additional compounds that act at dopamine receptors in other systems including quinperole (a D2 agonist) and raclopride (a D2 antagonist). Two of the mutants (eg643 and eg645) also exhibited reduced sensitivity to amphetamine. In behavioral assays, eg644 fails to slow upon re-entering a bacterial lawn. We are currently in the process of mapping and cloning the genes responsible for these mutant phenotypes.