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.

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

Steve Gendreau et al. (2002) West Coast Worm Meeting "Toward the identification of novel regulators of b-catenin signaling in C. elegans"

Emery Dora, Mike Costa, Damian Curtis, Lorena Mora-Blanco, Changyou Chen, Steve Gendreau

[West Coast Worm Meeting, 2002]

The unbridled transcriptional activation of Wnt-responsive genes is a frequent and early event in a number of human tumor types (Polakis, 2000). In an effort to identify novel regulators of Wnt-mediated signaling, we have initiated modifier screens in C. elegans around two key Wnt components, b-catenin (bar-1, Eisenman et al, 1998) and its negative regulator, axin (pry-1, Korswagen et al., 2002).

Palikaras K et al. (2016) Bio Protoc "Measuring Oxygen Consumption Rate in Caenorhabditis elegans."

Palikaras K, Tavernarakis N

[Bio Protoc, 2016]

The rate of oxygen consumption is a vital marker indicating cellular function during lifetime under normal or metabolically challenged conditions. It is used broadly to study mitochondrial function (Artal-Sanz and Tavernarakis, 2009; Palikaras et al., 2015; Ryu et al., 2016) or investigate factors mediating the switch from oxidative phosphorylation to aerobic glycolysis (Chen et al., 2015; Vander Heiden et al., 2009). In this protocol, we describe a method for the determination of oxygen consumption rates in the nematode Caenorhabditis elegans.

Chen CH et al. (2021) STAR Protoc "Live-cell imaging of PVD dendritic growth cone in post-embryonic C.elegans."

Chen CH, Pan CL

[STAR Protoc, 2021]

Live-cell imaging analysis provides tremendous information for the study of cellular events such as growth cone migration in neuronal development. Here, we describe a protocol for live-cell imaging of migrating PVD dendritic growth cones in the nematode <i>C.elegans</i> by spinning-disk confocal microscopy. Fluorescently labeled growth cones and cytoskeletal proteins could be continuously observed for 4-6h in mid-stage larvae. This protocol is suitable for revealing the dynamic molecular and cellular events in dendrite and axon development of <i>C.elegans</i>. For complete details on the use and execution of this protocol, please refer to Chen etal. (2019).

Mark Lackner et al. (2003) International Worm Meeting "Inhibiting Expression of Endosome-lysosome Docking Components Induces p53-independent and Caspase-dependent Apoptosis in C. elegans"

Mark Lackner, Rachel Kindt, Tak Hung, Changyou Chen, Dianne Parry, Mike Costa, Yvonne Franke, Carol OBrien

[International Worm Meeting, 2003]

We have isolated a nonsense mutant in the vps-41 gene that displays strong zygotic-effect induction of germline apoptosis, in addition to maternal-effect cytokinesis defects and embryonic arrest that are not associated with apoptosis. Apoptosis in the vps-41 mutant is blocked by a ced-4/APAF1 loss-of-function mutation, but not by a cep-1/p53 deletion, suggesting that loss of vps-41 activity induces the core apoptotic machinery independent of the DNA damage checkpoint. C. elegans vps-41 encodes the ortholog of human and yeast VPS41. S. cerevisiae VPS41 is required for sorting of proteins to the lysosome, and specifically for the step of endosomes docking to lysosomes prior to vesicle fusion. VPS41 forms a complex with four other scaffolding proteins (VPS11, VPS16, VPS18, and VPS33), as well as the Rab GEF protein VPS39. We identified a single C. elegans ortholog for each of the five other components of the endosome-lysosome docking (or HOPS) complex, and find that RNAi of each of these genes also strongly induces germline apoptosis in wildtype or in a cep-1/p53 deletion mutant, but not in ced-4/APAF1 or ced-3/caspase loss-of-function mutants. The yeast HOPS complex can also mediate docking of autophagosomes to lysosomes in the process of autophagy (degradation of cytoplasmic proteins and organelles), however RNAi of 12 homologs of yeast autophagy-specific genes does not induce germline apoptosis. RNAi of two additional genes that may be involved in lysosomal protein trafficking, as well as other functions, also induced germline apoptosis: an ortholog of human LAMPs (lysosome-associated transmembrane glycoproteins) and unc-32, a vacuolar (H+)-ATPase V0 domain a subunit. In one plausible model, blocking endosome docking to lysosomes might lead to the accumulation of unfused endosomes that ultimately rupture to release hydrolytic enzymes into the cytoplasm, damaging mitochondria and thereby triggering apoptosis. Since most cancer cells lack p53 function, and some also have increased protein synthesis and trafficking, inhibiting endosome-lysosome docking and fusion might provide a bypass mechanism for inducing apoptosis of tumor cells.

Memar, Nadin et al. (2022) MicroPubl Biol

Memar, Nadin, Lambie, Eric J, Sethi, Aditya, Luehr, Sebastian, Conradt, Barbara

[MicroPubl Biol, 2022]

Visualization of genomic loci with open chromatin state has been reported in mammalian tissue culture cells using a CRISPR/Cas9-based system that utilizes an EGFP-tagged endonuclease-deficient Cas9 protein (dCas9::EGFP) (Chen et al. 2013). Here, we adapted this approach for use in Caenorhabditis elegans . We generated a C. elegans strain that expresses the dCas9 protein fused to two nuclear-localized EGFP molecules (dCas9::NLS::2xEGFP::NLS) in an inducible manner. Using this strain, we report the visualization in live C. elegans embryos of two endogenous repetitive loci, rrn-4 and rrn-1 , from which 5S and 18S ribosomal RNAs are constitutively generated.