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| Status |
Public on May 01, 2020 |
| Title |
Diphthamide modification of eEF2 is required for gut tumor-like hyperplasia induced by oncogenic Ras |
| Organism |
Drosophila melanogaster |
| Experiment type |
Expression profiling by array
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| Summary |
Eukaryotic elongation factor 2 (eEF2) undergoes a unique post-translational modification called diphthamidation. Although eEF2 diphthamidation is highly conserved, its pathophysiological function is still largely unknown. To elucidate the function of diphthamidation in tumor, we examined the involvement of diphthamidation pathway enzyme Dph5 in tumor progression in Drosophila adult gut. Expression of oncogenic RasV12 in gut intestinal stem cells (ISCs) and enteroblasts (EBs) causes hypertrophy and disruption of gut epithelia, and shortened lifespan. Knockdown of dph5 ameliorated these pathogenic phenotypes. Dph5 is required for gross translation activation and high dMyc protein level in RasV12 tumor-like hyperplasia. Transcriptome analysis revealed that Dph5 is involved in the regulation of ribosome biogenesis genes. These results suggest that diphthamidation is required for translation activation partly through the regulation of ribosome biogenesis in Ras-induced tumor-like hyperplasia model in Drosophila gut.
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| Overall design |
Total RNA was extracted from the whole gut of each mutant adult flies (15 guts/sample) .N = 4 for each group.
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| Contributor(s) |
Sakurai KT, Kimura M, Miura M |
| Citation(s) |
31828897 |
| |
| Submission date |
Nov 29, 2019 |
| Last update date |
Aug 01, 2020 |
| Contact name |
Miura Masayuki |
| Organization name |
The University of Tokyo
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| Department |
Graduate School of Pharmaceutical Sciences
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| Lab |
Genetics Lab
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| Street address |
7-3-1 Hongo
|
| City |
Bunkyo-ku, Tokyo |
| ZIP/Postal code |
113-0033 |
| Country |
Japan |
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| Platforms (1) |
| GPL17277 |
Agilent-040871 Drosophila melanogaster 8X60K with Spike (Probe Name version) |
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| Samples (14)
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| Relations |
| BioProject |
PRJNA592564 |
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