Ching-Ming Wu

National Cheng Kung University; Tainan, Taiwan

CZ4734

Caenorhabditis elegans

CZ4733

Caenorhabditis elegans

CZ2475

Caenorhabditis elegans

Castillo-Quan JI et al. (2016) Cell "Metformin: Restraining Nucleocytoplasmic Shuttling to Fight Cancer and Aging."

Castillo-Quan JI, Blackwell TK

[Cell, 2016]

In this issue of Cell, Wu etal. employed C.elegans and human cell experiments to identify a pathway through which metformin increases lifespan and inhibits growth. A key transcriptional target, ACAD10, is activated when metformin induces nuclear exclusion of the GTPase RagC, thereby inhibiting mTORC1 through an unexpected mechanism.

Chou, Ting-Chen et al. (2011) International Worm Meeting "Characterization of the pathogenicity of Enterohaemorrhagic E. coli in C. elegans."

Chiu, Hao-Chieh, Chou, Ting-Chen, Chen, Chang-Shi, Wu, Ching-Ming, Kuo, Cheng-Ju

[International Worm Meeting, 2011]

Strains of Enterohaemorrhagic Escherichia coli (EHEC) that produce verocytotoxin, such as E. coli O157:H7, form an important group of zoonotic pathogens. E. coli O157:H7 has been implicated in large outbreaks as well as in sporadic cases of haemorrhagic colitis and the sometimes fatal haemolytic uremic syndrome. Here we applied the genetic tractable animal, C. elegans, as a model host to study the virulence of EHEC as well as the host innate immunity to this pathogen. Our preliminary data showed that EHEC intoxicated, induced severe Bag (bag-of-worms adults) phenotype, and eventually killed the worms. The transmission electron microscopy results indicated that EHEC induced attaching and effacing (A/E) lesions in the intestine. By further genetic analysis, we found that some important virulence factors of EHEC were required for its toxicity in C. elegans, and some conserved innate immune signal pathways were mediated in host susceptibility. Our results suggest that this EHEC-C. elegans model is suitable for future comprehensive genetic screens in both bacterial and host factors involved in the pathogenesis of EHEC.

Ji Wu et al. (2002) East Coast Worm Meeting "Regulation of Touch Cell Functional Genes"

Ji Wu, Martin Chalfie

[East Coast Worm Meeting, 2002]

We have previously shown that egl-44 and egl-46 are two transcription regulators involved in the development of several types of neurons in C. elegans, with significant homology in other organisms, and that they repress the expression of touch cell-specific features in FLP neurons (Wu et al., 2001,Genes. Dev., 15: 789).

Brissette B et al. (2019) Neuron "Insulin-like Peptides as Agents of Social Change."

Ringstad N, Brissette B

[Neuron, 2019]

Many behaviors promote reproduction or food finding. These critical functions of behavior can conflict; successful reproductive strategies can grow populations to the point where food is depleted. In this issue of Neuron, Wu etal. (2019) show how the nematode C.elegans detects crowding to change feeding behavior by coupling pheromone sensing to signaling via insulin-like peptides.

Wbp2nl

Homo sapiens

WBP2NL is a sperm-specific WW domain-binding protein that promotes meiotic resumption and pronuclear development during oocyte fertilization (Wu et al., 2007 [PubMed 17289678]).[supplied by OMIM, Mar 2008]

Wu D et al. (1997) Science "Interaction and regulation of subcellular localization of CED-4 by CED-9."

Wallen HD, Nunez G, Wu D

[Science, 1997]

The Caenorhabditis elegans survival gene ced-9 regulates ced-4 activity and inhibits cell death, but the mechanism by which this occurs is unknown. Through a genetic screen for CED-4-binding proteins, CED-9 was identified as an interacting partner of CED-4. CED-9, but not loss-of-function mutants, associated specifically with CED-4 in yeast or mammalian cells. The CED-9 protein localized primarily to intracellular membranes and the perinuclear region, whereas CED-4 was distributed in the cytosol. Expression of CED-9, but not a mutant lacking the carboxy-terminal hydrophobic domain, targeted CED-4 from the cytosol to intracellular membranes in mammalian cells. Thus, the actions of CED-4 and CED-9 are directly linked, which could provide the basis for the regulation of programmed cell death in C. elegans.AD - Department of Pathology and Comprehensive Cancer Center, The University of Michigan Medical School, Ann Arbor, MI 48109, USA.FAU - Wu, DAU - Wu DFAU - Wallen, H DAU - Wallen HDFAU - Nunez, GAU - Nunez GLA - engID - CA-64556/CA/NCIID - T32A107413-03/PHSPT - Journal ArticleCY - UNITED STATESTA - ScienceJID - 0404511RN - 0 (Calcium-Binding Proteins)RN - 0 (Ced-4 protein)RN - 0 (Ced-9 protein)RN - 0 (Helminth Proteins)RN - 0 (Proto-Oncogene Proteins)RN - 0 (bcl-x protein)SB - IM