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Disruption of Vps4 and JNK Function in Drosophila Causes Tumour Growth
| Content Provider | PubMed Central |
|---|---|
| Author | Rodahl, Lina M. Haglund, Kaisa Sem-jacobsen, Catherine Wendler, Franz Vincent, Jean-paul Lindmo, Karine Rusten, Tor Erik Stenmark, Harald |
| Editor | Blagosklonny, Mikhail V. |
| Copyright Year | 2009 |
| Abstract | Several regulators of endocytic trafficking have recently been identified as tumour suppressors in Drosophila. These include components of the endosomal sorting complex required for transport (ESCRT) machinery. Disruption of subunits of ESCRT-I and –II leads to cell-autonomous endosomal accumulation of ubiquitinated receptors, loss of apicobasal polarity and epithelial integrity, and increased cell death. Here we report that disruption of the ATPase dVps4, the most downstream component of the ESCRT machinery, causes the same array of cellular phenotypes. We find that loss of epithelial integrity and increased apoptosis, but not loss of cell polarity, require the activation of JNK signalling. Abrogation of JNK signalling prevents apoptosis in dVps4 deficient cells. Indeed double deficiency in dVps4 and JNK signalling leads to the formation of neoplastic tumours. We conclude that dvps4 is a tumour suppressor in Drosophila and that JNK is central to the cell-autonomous phenotypes of ESCRT-deficient cells. |
| Related Links | http://dx.doi.org/10.1371/journal.pone.0004354 |
| Starting Page | 4354 |
| File Format | |
| ISSN | 19326203 |
| e-ISSN | 19326203 |
| Journal | PLoS ONE |
| Issue Number | 2 |
| Volume Number | 4 |
| Language | English |
| Publisher | Public Library of Science |
| Access Restriction | Open |
| Rights Holder | Public Library of Science |
| Subject Keyword | Research in Higher Education |
| Content Type | Text |
| Resource Type | Article |
| Subject | Multidisciplinary |
