Huang, Huiyan et al. (2013) Worm Breeder's Gazette "How to measure lethargus quiescence without monopolizing the dissection microscopes in your lab"

Zhu, Chen-Tseh, Hart, Anne, Huang, Huiyan

[Worm Breeder's Gazette, 2013]

Melander RJ et al. (2015) Chem Biol "From worms to targeting virulence factors."

Melander C, Melander RJ

[Chem Biol, 2015]

Rising antibiotic resistance means that alternative antibacterial strategies are sorely needed. In this issue, Zhu etal. (2015) report the use of a Caenorhabditis elegans model to validate the Pseudomonas aeruginosa virulence factor LasB as a potential therapeutic target and to identify a LasB inhibitor with invivo efficacy.

Yeh CY et al. (2021) Dev Cell "A leucine-derived fatty acid unlocks the mTOR to development."

Yeh CY, Lamming DW

[Dev Cell, 2021]

Understanding how nutrient-sensitive signaling pathways regulate development and aging is an active area of research. In this issue of Developmental Cell,Zhu and colleagues (2021) identify a specific monomethylated branched-chain fatty acid that overrides nutrient deprivation signaling and activates mTORC1 in C.elegans and mammalian cells.

Po MD et al. (2012) Neuron "Releasing the inner inhibition for axon regeneration."

Po MD, Calarco JA, Zhen M

[Neuron, 2012]

The adult mammalian central nervous system exhibits restricted regenerative potential. Chen etal. (2011) and El Bejjani and Hammarlund (2012) used Caenorhabditis elegans to uncover intrinsic factors that inhibit regeneration of axotomized mature neurons, opening avenues for potential therapeutics.

Molinie N et al. (2016) Dev Cell "WASP and WAVE Team Up at the Leading Edge."

Molinie N, Gautreau A

[Dev Cell, 2016]

Arp2/3-dependent branched actin networks drive membrane protrusions, with WAVE being recognized as the critical Arp2/3 activator in this process. In this issue of Developmental Cell, Zhu etal. (2016) demonstrate that WASP, an Arp2/3 activator mostly involved in endocytosis, collaborates with WAVE to promote migration of neuroblasts in Caenorhabditis elegans.

Huang, Huiyan et al. (2015) International Worm Meeting "NCA sodium leak channels and gap junctions regulate sleep and arousal in C. elegans."

Huang, Huiyan, Zhu, Chen-Tseh, Bennett, Heather, Skuja, Lukas, Hart, Anne, Hayden, Dustin

[International Worm Meeting, 2015]

During sleep, animals exhibit a heightened arousal threshold and decreased behavioral response to external stimuli. The molecular and cellular mechanisms underlying these changes are not fully understood. We report here that the activity of the C. elegans NALCN sodium leak channel, NCA, is critical for normal sleep and arousal. Sodium leak channels regulate resting membrane potential, thus contributing to the overall neuronal excitability (PMID:17448995, PMID:23522043). We found that diminished NCA activity in C. elegans robustly increased arousal threshold during sleep bouts in L4-to-adult lethargus, consistent with decreased excitability. Quantity of sleep was only modestly increased in these animals, whereas heightened NCA activity dramatically decreased sleep. Loss of cGMP-dependent protein kinase EGL-4 suppressed NCA loss of function defects. This suggests a model in which increased arousal threshold during sleep requires down-regulation of the sodium leak channel, which, directly or indirectly, activates the EGL-4 protein kinase. Others have suggested that Drosophila sodium leak channel drives the pigment dispersing factor (PDF) neuropeptide release, regulating daily rhythmic behavior (PMID:16364900, PMID:20362452). However, in C. elegans, losing PDF-1, one of the two PDF neuropeptides, had no impact on animals with increased NCA function. Intriguingly, loss of the PDF receptor increased arousal threshold, reminiscent of decreased NCA function.NCA channels, cooperatively with gap junctions, are required for normal response to general anesthetics (PMID:3576211) and function in the premotor interneurons to regulate neuronal excitability (PMID:25716181, PMID: 21489288). Consistent with these findings, loss of UNC-7 or UNC-9 gap junction proteins partially suppressed the increased sleep of animals with diminished NCA function. Moreover, loss of UNC-7 in premotor interneurons or loss of UNC-9 in motor neurons significantly decreased sleep and lowered arousal threshold during sleep. Conversely, overexpressing UNC-7 and UNC-9 in adult animals was sufficient to induce anachronistic sleep. Combined, these results emphasize the conservation and importance of neuronal activity during sleep, demonstrate a role for gap junctions in sleep, and identify possible targets for the modulation of sleep entry and maintenance.

Silverstein NJ et al. (2017) Immunity "Interleukin-17: Why the Worms Squirm."

Huh JR, Silverstein NJ

[Immunity, 2017]

IL-17 is a cytokine known primarily for its role in inflammation. In a recent issue of Nature, Chen etal. (2017) demonstrate that IL-17 plays a neuromodulatory role in Caenorhabditis elegans by acting directly on neurons to amplify neuronal responses to stimuli and produce changes in animal behavior.

Artan M et al. (2016) Dev Cell "Heat FLiPs a Hormonal Switch for Longevity."

Lee SV, An SW, Artan M

[Dev Cell, 2016]

Temperature-sensing neurons in C.elegans reduce the life-shortening effects of high temperatures via steroid signaling. In this issue of Developmental Cell, Chen etal. (2016) elucidate the underlying mechanisms by which the transcription factor CREB induces the neuropeptide FLP-6 in the temperature-sensing neurons to counteract the life-shortening effects of high temperature.

Akin O et al. (2014) Cell "The shape of things to come."

Akin O, Zipursky SL

[Cell, 2014]

Surface receptors can link binding of ligands to changes in the actin-based cell cytoskeleton. Chia etal. and Chen etal. provide evidence for direct binding between the cytoplasmic tails ofreceptorsand the WAVE complex, a regulator of the actin nucleator Arp2/3 complex, which mighthelp to explain how environmental signals are translated into changes in morphology andmotility.

Chen X et al. (2015) Mol Neurodegener "Erratum to: Ethosuximide ameliorates neurodegenerative disease phenotypes by modulating DAF-16/FOXO target gene expression."

McCue HV, Chen X, Morgan A, Kashyap SS, Barclay JW, Kraemer BC, Burgoyne RD, Wong SQ

[Mol Neurodegener, 2015]

The original version of this article [1] unfortunately contained a mistake. The author list contained a spelling error for the author Hannah V. McCue. The original article has been corrected for this error. The corrected author list is given below:Xi Chen, Hannah V. McCue, Shi Quan Wong, Sudhanva S. Kashyap, Brian C. Kraemer, Jeff W. Barclay, Robert D. Burgoyne and Alan Morgan