Chang JT et al. (2020) Methods Mol Biol "Correction to: Assessing Tissue-Specific Autophagy Flux in Adult Caenorhabditis elegans."

Chang JT, Kumsta C, Hansen M

[Methods Mol Biol, 2020]

Correction to: Chapter 17 in: Sean P. Curran (ed.), Aging: Methods and Protocols, Methods in Molecular Biology, vol. 2144.

Eddy SR (1994) Worm Breeder's Gazette "Three Families of Reverse Transcriptase Elements in C. elegans"

Eddy SR

[Worm Breeder's Gazette, 1994]

Three families of reverse transcriptase elements in C. elegans Sean Eddy, MRC-LMB, Hills Road, Cambridge CB2 2QH, UK

Yu, Xupeng et al. (2021) International Worm Meeting "Characterising single-stranded telomere binding proteins in C. elegans"

Ferreira, Helder, Gray, Sean, Yu, Xupeng

[International Worm Meeting, 2021]

Telomeres are nucleoprotein complexes that protect the ends of linear chromosomes. Loss of telomere capping activates the DNA damage response, normally resulting in senescence or apoptosis. C. elegans telomeres are unusual in that they end in C-rich single-stranded DNA overhangs as well as the more common G-rich single-stranded DNA overhangs. Distinct proteins, namely POT-1 and POT-2, bind these different overhangs. However, neither of these proteins are essential, which suggests that there may be other telomeric single-stranded DNA binding proteins in worms. We characterise POT-3 as a single OB-fold containing protein that specifically binds the G-rich telomere strand with remarkable selectivity and affinity. We map its minimal DNA recognition sequence to a 6nt GCTTAG sequence. Strikingly, POT-3 and POT-2 bind precisely the same minimal nucleotide sequence but POT-3 has higher selectivity when the GCTTAG recognition sequence is at the extreme 3' hydroxyl end. We believe that POT-3's ability to cap the terminal end of the G-overhang mediates a unique telomeric function.

Antol, Weronika et al. (2022) MicroPubl Biol

Sychta, Karolina, Prokop, Zofia M., Antol, Weronika, Palka, Joanna K., Dudek, Katarzyna

[MicroPubl Biol, 2022]

Caenorhabditis elegans is a model species, increasingly used in experimental evolution studies to investigate such major topics as: maintenance of genetic variation, host-pathogen interaction and coevolution, mutations, life history, evolution of reproductive systems, sexual selection (Gray and Cutter, 2014; Teotnio, Estes, Phillips, and Baer, 2017). Its reproductive system in the wild, known as androdioecy, involves mostly self-fertilization of hermaphrodites and occasionally outcrossing with males, which are generally rare (Stewart and Phillips, 2002). This system can be experimentally changed to dioecy, i.e., obligatory outcrossing, through genetic manipulations (see Table I in Anderson, Morran, and Phillips, 2010; Gray and Cutter, 2014).

Chalasani, Sreekanth H. et al. (2009) International Worm Meeting "AWC sensory neurons release two neurotransmitters to regulate exploratory behavior upon removal from food."

Albrecht, Dirk, Bargmann, Cornelia I., Chalasani, Sreekanth H., Kato, Saul

[International Worm Meeting, 2009]

Animals increase their pirouette frequency in response to removal from food stimulus for a period of 15 min. The AWC and ASK sensory neurons and the AIB interneurons stimulate pirouettes immediately after removal from food, while the AIY and AIA interneurons inhibit pirouettes (Wakabayashi et al 2004, Gray et al 2005). We have found that AWC sensory neurons become active in response to removal of stimulus, releasing two neurotransmitters (glutamate and a neuropeptide NLP-1). The released glutamate acts to activate AIB and inhibit AIY interneurons, promoting reversals (Chalasani et al 2007). In contrast to glutamate, AWC-released NLP-1 acts on AIA interneurons to suppress reversals, suggesting that reversal frequencies are regulated by at least two opposing signaling systems. AWC calcium responses are modulated in these neurotransmitter mutants, suggesting that feedback pathways affect AWC neuronal activity. References: Chalasani, S. H., Chronis, N., Tsunozaki, M., Gray, J. M., Ramot, D., Goodman, M. B., and Bargmann, C. I. (2007). Dissecting a circuit for olfactory behaviour in Caenorhabditis elegans. Nature 450, 63-70. Gray, J.M., Hill, J.J., and Bargmann, C.I. (2005). A circuit for navigation in Caenorhabditis elegans. Proc. Natl. Acad. Sci. 102, 3184-3191. Wakabayashi, T., Kitagawa, I., and Shingai, R. (2004). Neurons regulating the duration of forward locomotion in Caenorhabditis elegans. Neurosci. Res. 50, 103-111.

Avery L (1995) Worm Breeder's Gazette "Effects of Conus venoms on the pharynx"

Avery L

[Worm Breeder's Gazette, 1995]

Cone snails are predatory snails. They harpoon their prey, which may be small fish, marine worms, or other snails, then inject a paralyzing venom through the hollow harpoon (Olivera et al, Science 249: 257). The venom is a complex mixture of tiny peptide toxins, different in each species. Several of these toxins have been shown to act on cell-surface molecules important for nervous system function such as the N-type Ca++ channel or the voltage-gated Na+ channel (Gray et al, Ann Rev Biochem 57: 665).

Chalasani S H et al. (2010) Neuronal Development, Synaptic Function and Behavior, Madison, WI "Neuropeptide feedback modifies odor induced responses in Caenorhabditis elegans olfactory neurons"

Bargmann C I, Kato S, Chalasani S H, Albrecht D R

[Neuronal Development, Synaptic Function and Behavior, Madison, WI, 2010]

Neural circuits transform sensory signals to generate behaviors on timescales from seconds to hours. In some C.elegans behaviors, sensory inputs lead to long lasting and complex behavioral outputs. Animals that have been removed from food spend about 15 minutes exploring a local area by interrupting long forward movements with reversals and turns (Wakabayashi et al., 2004, Gray et al 2005). AWC sensory neurons regulate this behavior by releasing two neurotransmitters, glutamate (promoting turns) and NLP-1 (inhibiting turns). AWC sensory neuron released glutamate activates AIB and inhibits AIY and AIA interneurons (Chalasani et al 2007). In contrast to glutamate, AWC neuron released NLP-1 acts on AIA interneurons to suppress reversals, indicating that turn frequencies are regulated by at least two opposing systems. AWC calcium responses are modulated in these neurotransmitter mutants suggesting that multiple pathways can influence AWC dependent behavior and neuronal activity. ReferencesChalasani, S. H., et. al. Dissecting a neural circuit for olfactory behaviour in Caenorhabditis elegans. Nature 450, 63-70 (2007).Gray, J.M., et. al. A circuit for navigation in Caenorhabditis elegans. Proc. Natl. Acad. Sci. 102, 3184-3191 (2005).Wakabayashi, T., et. al. Neurons regulating the duration of forward locomotion in Caenorhabditis elegans. Neurosci. Res. 50, 103-111 (2004).

Zhang H et al. (2008) Mol Biol Cell "RAB-11 permissively regulates spindle alignment by modulating metaphase microtubule dynamics in Caenorhabditis elegans early embryos."

Zhang H, White JG, Squirrell JM

[Mol Biol Cell, 2008]

Monitoring Editor: Sean Munro Alignment of the mitotic spindle along a pre-formed axis of polarity is crucial for generating cell diversity in many organisms (Segal and Bloom, 2001; Betschinger and Knoblich, 2004), yet little is known about the role of the endomembrane system in this process. RAB-11 is a small GTPase enriched in recycling endosomes. When we depleted RAB-11 by RNAi in C. elegans, the spindle of the one-cell embryo failed to align along the axis of polarity in metaphase and underwent violent movements in anaphase. The distance between astral microtubules ends and the anterior cortex was significantly increased in rab-11(RNAi) embryos specifically during metaphase, possibly accounting for the observed spindle alignment defects. Additionally, we found that normal ER morphology requires functional RAB-11, particularly during metaphase. We hypothesize that RAB-11, in conjunction with the ER, acts to regulate cell cycle specific changes in astral microtubule length to ensure proper spindle alignment in C. elegans early embryos.

Sreekanth Chalasani et al. (2007) International Worm Meeting "Functional analysis of a neural circuit controlling turning behavior in Caenorhabditis elegans."

Cornelia Bargmann, Jesse Gray, Makoto Tsunozaki, Sreekanth Chalasani, Nikolas Chronis

[International Worm Meeting, 2007]

C. elegans increase its frequency of reversals and turns (jointly termed pirouettes, Pierce-Shimomura et al 1999) after removal of a food stimulus. The AWC and ASK sensory neurons and the AIB interneurons stimulate pirouettes immediately after removal from food, while the AIY and AIA interneurons inhibit pirouettes (Wakabayashi et al 2004, Gray et al 2005). We have found that the sensory neuron AWC releases two neurotransmitters (glutamate and a neuropeptide, NLP-1) when the worm is removed from food. The released glutamate acts to activate AIB and inhibit AIY, promoting reversals. Strains with different reversal frequencies can be generated by manipulating the level of glutamate receptors on interneurons AIB and AIY. Decreasing receptor expression leads to fewer reversals, and increasing receptor expression results in more reversals than in wild-type. The AWC released neuropeptide NLP-1 serves to reduce reversals, suggesting that reversal frequencies are regulated by at least two opposing signaling systems. Consistent with behavioral responses, AWC and AIB respond (by increasing calcium concentration) to removal of stimulus. We plan to extend the imaging studies to other neurons in the circuit. These results provide a plausible molecular explanation that links neurotransmitters, their receptors, and neuronal circuitry to generate behavior. References: Gray, J.M., Hill, J.J., and Bargmann, C.I. (2005). A circuit for navigation in Caenorhabditis elegans. Proc. Natl. Acad. Sci. 102, 3184-3191. Pierce-Shimomura, J.T., Morse, T.M., and Lockery, S.R. (1999). The fundamental role of pirouettes in Caenorhabditis elegans chemotaxis. J. Neurosci 19, 9557-9569. Wakabayashi, T., Kitagawa, I., and Shingai, R. (2004). Neurons regulating the duration of forward locomotion in Caenorhabditis elegans. Neurosci. Res. 50, 103-111.

McEwen JM et al. (2008) Mol Biol Cell "UNC-18 promotes both the anterograde trafficking and synaptic function of syntaxin."

Kaplan JM, McEwen JM

[Mol Biol Cell, 2008]

Monitoring Editor: Sean Munro The SM protein UNC-18 has been proposed to regulate several aspects of secretion, including synaptic vesicle (SV) docking, priming, and fusion. Here we show that UNC-18 has a chaperone function in neurons, promoting anterograde transport of the plasma membrane SNARE protein Syntaxin-1. In unc-18 mutants, UNC-64 (C. elegans Syntaxin-1) accumulates in neuronal cell bodies. Colocalization studies and analysis of carbohydrate modifications both suggest that this accumulation occurs in the endoplasmic reticulum. This trafficking defect is specific for UNC-64 Syntaxin-1, as 14 other SNARE proteins and 2 active zone markers were unaffected. UNC-18 binds to Syntaxin through at least two mechanisms: binding to closed Syntaxin, or to the N-terminus of Syntaxin. It is unclear which of these binding modes mediates UNC-18 function in neurons. The chaperone function of UNC-18 was eliminated in double mutants predicted to disrupt both modes of Syntaxin binding, but was unaffected in single mutants. By contrast, mutations predicted to disrupt UNC-18 binding to the N-terminus of Syntaxin caused significant defects in locomotion behavior and responsiveness to cholinesterase inhibitors. Collectively, these results demonstrate the UNC-18 acts as a molecular chaperone for Syntaxin transport in neurons, and that the two modes of UNC-18 binding to Syntaxin are involved in different aspects of UNC-18 function.