scholarly journals Cell Corpse Engulfment Mediated by C. elegans Phosphatidylserine Receptor Through CED-5 and CED-12

Science ◽  
2003 ◽  
Vol 302 (5650) ◽  
pp. 1563-1566 ◽  
Author(s):  
X. Wang
Keyword(s):  
C Elegans ◽  
Phosphatidylserine Receptor ◽  
Cell Corpse ◽  
Corpse Engulfment

scholarly journals CED-10-WASP-Arp2/3 signaling axis regulates apoptotic cell corpse engulfment in C. elegans

2017 ◽  
Vol 428 (1) ◽  
pp. 215-223 ◽  
Author(s):  
Dou Wu ◽  
Yongping Chai ◽  
Zhiwen Zhu ◽  
Wenjing Li ◽  
Guangshuo Ou ◽  
...  
Keyword(s):  
Apoptotic Cell ◽  
C Elegans ◽  
Signaling Axis ◽  
Cell Corpse ◽  
Corpse Engulfment

scholarly journals 6-OHDA-induced dopaminergic neurodegeneration in C. elegans is promoted by the engulfment pathway and inhibited by the transthyretin-related protein TTR-33

2017 ◽  
Author(s):  
Sarah-Lena Offenburger ◽  
Xue Yan Ho ◽  
Theresa Tachie-Menson ◽  
Sean Coakley ◽  
Massimo A. Hilliard ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dopaminergic Neurons ◽  
Oxygen Species ◽  
Related Protein ◽  
Mapk Kinase ◽  
C Elegans ◽  
Dopaminergic Neurodegeneration ◽  
Cell Corpse ◽  
6 Hydroxydopamine ◽  
Corpse Engulfment

AbstractOxidative stress is linked to many pathological conditions including the loss of dopaminergic neurons in Parkinson’s disease. The vast majority of disease cases appear to be caused by a combination of genetic mutations and environmental factors. We screened for genes protecting Caenorhabditis elegans dopaminergic neurons from oxidative stress induced by the neurotoxin 6-hydroxydopamine (6-OHDA) and identified the transthyretin-related gene ttr-33. The only described C. elegans transthyretin-related protein to date, TTR-52, has been shown to mediate corpse engulfment as well as axon repair. We demonstrate that TTR-52 and TTR-33 have distinct roles. TTR-33 is likely produced in the posterior arcade cells in the head of C. elegans larvae and is predicted to be a secreted protein. TTR-33 protects C. elegans from oxidative stress induced by paraquat or H2O2 at an organismal level. The increased oxidative stress sensitivity of ttr-33 mutants is alleviated by mutations affecting the KGB-1 MAPK kinase pathway, whereas it is enhanced by mutation of the JNK-1 MAPK kinase. Finally, we provide genetic evidence that the C. elegans cell corpse engulfment pathway is required for the degeneration of dopaminergic neurons after exposure to 6-OHDA. In summary, we describe a new neuroprotective mechanism and demonstrate that TTR-33 normally functions to protect dopaminergic neurons from oxidative stress-induced degeneration, potentially by acting as a secreted sensor or scavenger of oxidative stress.Author summaryAnimals employ multiple mechanisms to prevent their cells from damage by reactive oxygen species, chemically reactive molecules containing oxygen. Oxidative stress, caused by the overabundance of reactive oxygen species or a decreased cellular defence against these chemicals, is linked to a variety of neurodegenerative conditions, including the loss of dopaminergic neurons in Parkinson’s disease. In this study, we discovered a novel protective molecule that functions to prevent dopaminergic neurodegeneration caused by oxidative stress induced by the neurotoxin 6-hydroxydopamine (6-OHDA). We used the nematode C. elegans, a well-characterised model in which mechanisms can be studied on an organismal level. When C. elegans is exposed to 6-OHDA, its dopaminergic neurons gradually die. Our major findings include (i) mutations of the transthyretin-related gene ttr-33 causes highly increased dopaminergic neurodegeneration after 6-OHDA exposure; (ii) TTR-33 is likely produced and secreted by several cells in the head of the animal; (iii) TTR-33 protects against oxidative stress induced by other compounds; (iv) mutations in the KGB-1 MAP kinase stress pathway alleviate dopaminergic neuron loss in the ttr-33 mutant; and (v) the cell corpse engulfment pathway is required for dopaminergic neurodegeneration. We hypothesise that TTR-33 protects dopaminergic neurons against 6-OHDA-induced oxidative stress by acting as an oxygen sensor or scavenger.

scholarly journals C. elegans Secreted Lipid-Binding Protein NRF-5 Mediates PS Appearance on Phagocytes for Cell Corpse Engulfment

2012 ◽  
Vol 22 (14) ◽  
pp. 1276-1284 ◽  
Author(s):  
Yan Zhang ◽  
Haibin Wang ◽  
Eriko Kage-Nakadai ◽  
Shohei Mitani ◽  
Xiaochen Wang
Keyword(s):  
Binding Protein ◽  
Lipid Binding ◽  
Lipid Binding Protein ◽  
C Elegans ◽  
Cell Corpse ◽  
Corpse Engulfment

scholarly journals The C. elegans Cell Corpse Engulfment Gene ced-7 Encodes a Protein Similar to ABC Transporters

Cell ◽  
1998 ◽  
Vol 93 (6) ◽  
pp. 951-960 ◽  
Author(s):  
Yi-Chun Wu ◽  
H.Robert Horvitz
Keyword(s):  
Abc Transporters ◽  
C Elegans ◽  
Cell Corpse ◽  
Corpse Engulfment

scholarly journals C. elegans CED-12 Acts in the Conserved CrkII/DOCK180/Rac Pathway to Control Cell Migration and Cell Corpse Engulfment

2001 ◽  
Vol 1 (4) ◽  
pp. 491-502 ◽  
Author(s):  
Yi-Chun Wu ◽  
Miao-Chih Tsai ◽  
Li-Chun Cheng ◽  
Chung-Jung Chou ◽  
Nei-Yin Weng
Keyword(s):  
Cell Migration ◽  
Control Cell ◽  
C Elegans ◽  
Cell Corpse ◽  
Corpse Engulfment

scholarly journals CED-1 Is a Transmembrane Receptor that Mediates Cell Corpse Engulfment in C. elegans

Cell ◽  
2001 ◽  
Vol 104 (1) ◽  
pp. 43-56 ◽  
Author(s):  
Zheng Zhou ◽  
Erika Hartwieg ◽  
H.Robert Horvitz
Keyword(s):  
C Elegans ◽  
Cell Corpse ◽  
Corpse Engulfment

scholarly journals Three C. elegans Rac proteins and several alternative Rac regulators control axon guidance, cell migration and apoptotic cell phagocytosis

Development ◽  
2001 ◽  
Vol 128 (22) ◽  
pp. 4475-4488 ◽  
Author(s):  
Erik A. Lundquist ◽  
Peter W. Reddien ◽  
Erika Hartwieg ◽  
H. Robert Horvitz ◽  
Cornelia I. Bargmann
Keyword(s):  
Cell Migration ◽  
Axon Guidance ◽  
Apoptotic Cell ◽  
Regulatory Proteins ◽  
Axon Pathfinding ◽  
C Elegans ◽  
Cell Corpse ◽  
And Function ◽  
Redundant Functions ◽  
Caenorhabditis Elegans Genome

The Caenorhabditis elegans genome contains three rac-like genes, ced-10, mig-2, and rac-2. We report that ced-10, mig-2 and rac-2 act redundantly in axon pathfinding: inactivating one gene had little effect, but inactivating two or more genes perturbed both axon outgrowth and guidance. mig-2 and ced-10 also have redundant functions in some cell migrations. By contrast, ced-10 is uniquely required for cell-corpse phagocytosis, and mig-2 and rac-2 have only subtle roles in this process. Rac activators are also used differentially. The UNC-73 Trio Rac GTP exchange factor affected all Rac pathways in axon pathfinding and cell migration but did not affect cell-corpse phagocytosis. CED-5 DOCK180, which acts with CED-10 Rac in cell-corpse phagocytosis, acted with MIG-2 but not CED-10 in axon pathfinding. Thus, distinct regulatory proteins modulate Rac activation and function in different developmental processes.

scholarly journals Requirement of Adaptor Protein GULP during Stabilin-2-mediated Cell Corpse Engulfment

2008 ◽  
Vol 283 (16) ◽  
pp. 10593-10600 ◽  
Author(s):  
Seung-Yoon Park ◽  
Kae-Bok Kang ◽  
Narendra Thapa ◽  
Sang-Yeob Kim ◽  
Sung-Jin Lee ◽  
...  
Keyword(s):  
Adaptor Protein ◽  
Cell Corpse ◽  
Corpse Engulfment
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