Source:http://linkedlifedata.com/resource/pubmed/id/10200472
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
4
|
| pubmed:dateCreated |
1999-5-11
|
| pubmed:abstractText |
We studied the role of Ras signaling in the regulation of cell death during Drosophila eye development. Overexpression of Argos, a diffusible inhibitor of the EGF receptor and Ras signaling, caused excessive cell death in developing eyes at pupal stages. The Argos-induced cell death was suppressed by coexpression of the anti-apoptotic genes p35, diap1, or diap2 in the eye as well as by the Df(3L)H99 chromosomal deletion that lacks three apoptosis-inducing genes, reaper, head involution defective (hid) and grim. Transient misexpression of the activated Ras1 protein (Ras1V12) later in pupal development suppressed the Argos-induced cell death. Thus, Argos-induced cell death seemed to have resulted from the suppression of the anti-apoptotic function of Ras. Conversely, cell death induced by overexpression of Hid was suppressed by gain-of-function mutations of the genes coding for MEK and ERK. These results support the idea that Ras signaling functions in two distinct processes during eye development, first triggering the recruitment of cells and later negatively regulating cell death.
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| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Argos protein, Drosophila,
http://linkedlifedata.com/resource/pubmed/chemical/Caspases,
http://linkedlifedata.com/resource/pubmed/chemical/Drosophila Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Eye Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Insect Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Nerve Tissue Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/ras Proteins
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| pubmed:status |
MEDLINE
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| pubmed:month |
Apr
|
| pubmed:issn |
1350-9047
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| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
5
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
262-70
|
| pubmed:dateRevised |
2008-11-21
|
| pubmed:meshHeading |
pubmed-meshheading:10200472-Animals,
pubmed-meshheading:10200472-Animals, Genetically Modified,
pubmed-meshheading:10200472-Apoptosis,
pubmed-meshheading:10200472-Caspases,
pubmed-meshheading:10200472-Drosophila,
pubmed-meshheading:10200472-Drosophila Proteins,
pubmed-meshheading:10200472-Eye,
pubmed-meshheading:10200472-Eye Proteins,
pubmed-meshheading:10200472-Gene Expression Regulation, Developmental,
pubmed-meshheading:10200472-Genes, Insect,
pubmed-meshheading:10200472-Insect Proteins,
pubmed-meshheading:10200472-Microscopy, Electron, Scanning,
pubmed-meshheading:10200472-Nerve Tissue Proteins,
pubmed-meshheading:10200472-Phenotype,
pubmed-meshheading:10200472-Promoter Regions, Genetic,
pubmed-meshheading:10200472-Pupa,
pubmed-meshheading:10200472-Signal Transduction,
pubmed-meshheading:10200472-ras Proteins
|
| pubmed:year |
1998
|
| pubmed:articleTitle |
Argos induces programmed cell death in the developing Drosophila eye by inhibition of the Ras pathway.
|
| pubmed:affiliation |
Department of Neuroanatomy, Biomedical Research Center, Osaka University Medical School, and CREST, Japan Science and Technology Corporation (JST), 2-2 Yamadaoka, Suita, Osaka 565, Japan.
|
| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|