Diphthamide modification of eEF2 is required for gut tumor‐like hyperplasia induced by oncogenic Ras
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 involve...
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| Veröffentlicht in: | Genes to cells : devoted to molecular & cellular mechanisms 2020-02, Vol.25 (2), p.76-85 |
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| creator | Tsuda‐Sakurai, Kayoko Kimura, Masaki Miura, Masayuki |
| description | 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 life span. 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.
Expression of oncogenic RasV12 in gut intestinal stem cells (ISCs) and enteroblasts (EBs) causes hypertrophy and disruption of gut epithelia and shortened life span. Knockdown of Dph5 ameliorated these pathogenic phenotypes. |
| doi_str_mv | 10.1111/gtc.12742 |
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Expression of oncogenic RasV12 in gut intestinal stem cells (ISCs) and enteroblasts (EBs) causes hypertrophy and disruption of gut epithelia and shortened life span. Knockdown of Dph5 ameliorated these pathogenic phenotypes.</description><identifier>ISSN: 1356-9597</identifier><identifier>EISSN: 1365-2443</identifier><identifier>DOI: 10.1111/gtc.12742</identifier><identifier>PMID: 31828897</identifier><language>eng</language><publisher>England: Wiley Subscription Services, Inc</publisher><subject>Biosynthesis ; Digestive system ; diphthamidation ; Drosophila ; Gastrointestinal tract ; Gene expression ; Gene regulation ; Hyperplasia ; Hypertrophy ; Insects ; Intestine ; Life span ; Myc ; Phenotypes ; Ras ; Ras protein ; Stem cells ; Translation ; tumor</subject><ispartof>Genes to cells : devoted to molecular & cellular mechanisms, 2020-02, Vol.25 (2), p.76-85</ispartof><rights>2019 Molecular Biology Society of Japan and John Wiley & Sons Australia, Ltd</rights><rights>2019 Molecular Biology Society of Japan and John Wiley & Sons Australia, Ltd.</rights><rights>2020 Molecular Biology Society of Japan and John Wiley & Sons Australia, Ltd</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4542-9ea943408dc3148dc84665a355a6883bbdbc8bf6a1c3197d1700c64295ed2a6e3</citedby><cites>FETCH-LOGICAL-c4542-9ea943408dc3148dc84665a355a6883bbdbc8bf6a1c3197d1700c64295ed2a6e3</cites><orcidid>0000-0001-7444-5705</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fgtc.12742$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fgtc.12742$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1416,1432,27923,27924,45573,45574,46408,46832</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31828897$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tsuda‐Sakurai, Kayoko</creatorcontrib><creatorcontrib>Kimura, Masaki</creatorcontrib><creatorcontrib>Miura, Masayuki</creatorcontrib><title>Diphthamide modification of eEF2 is required for gut tumor‐like hyperplasia induced by oncogenic Ras</title><title>Genes to cells : devoted to molecular & cellular mechanisms</title><addtitle>Genes Cells</addtitle><description>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 life span. 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.
Expression of oncogenic RasV12 in gut intestinal stem cells (ISCs) and enteroblasts (EBs) causes hypertrophy and disruption of gut epithelia and shortened life span. Knockdown of Dph5 ameliorated these pathogenic phenotypes.</description><subject>Biosynthesis</subject><subject>Digestive system</subject><subject>diphthamidation</subject><subject>Drosophila</subject><subject>Gastrointestinal tract</subject><subject>Gene expression</subject><subject>Gene regulation</subject><subject>Hyperplasia</subject><subject>Hypertrophy</subject><subject>Insects</subject><subject>Intestine</subject><subject>Life span</subject><subject>Myc</subject><subject>Phenotypes</subject><subject>Ras</subject><subject>Ras protein</subject><subject>Stem cells</subject><subject>Translation</subject><subject>tumor</subject><issn>1356-9597</issn><issn>1365-2443</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><recordid>eNp10MtKxDAUBuAgiveFLyABN7qo09zaZinjFQRBdF3S5HQm2jY1aZHZ-Qg-o09ixlEXglmcBPLxc_gROiDpKYlnMhv0KaE5p2tom7BMJJRztr58iyyRQuZbaCeEpzQljKZiE20xUtCikPk2qs9tPx_mqrUGcOuMra1Wg3UddjWGi0uKbcAeXkbrweDaeTwbBzyMrfMfb--NfQY8X_Tg-0YFq7DtzKgjrBbYddrNoLMa36uwhzZq1QTY_7530ePlxcP0Orm9u7qZnt0mmgtOEwlKcsbTwmhGeJwFzzKhmBAqKwpWVabSRVVnisR_mRuSp6nOOJUCDFUZsF10vMrtvXsZIQxla4OGplEduDGUlFFBpRQ5i_ToD31yo-_idlFFRKTMaVQnK6W9C8FDXfbetsovSpKWy_LLWH75VX60h9-JY9WC-ZU_bUcwWYFX28Di_6Ty6mG6ivwEV2qOWQ</recordid><startdate>202002</startdate><enddate>202002</enddate><creator>Tsuda‐Sakurai, Kayoko</creator><creator>Kimura, Masaki</creator><creator>Miura, Masayuki</creator><general>Wiley Subscription Services, Inc</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TK</scope><scope>7TM</scope><scope>8FD</scope><scope>FR3</scope><scope>M7N</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0001-7444-5705</orcidid></search><sort><creationdate>202002</creationdate><title>Diphthamide modification of eEF2 is required for gut tumor‐like hyperplasia induced by oncogenic Ras</title><author>Tsuda‐Sakurai, Kayoko ; Kimura, Masaki ; Miura, Masayuki</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4542-9ea943408dc3148dc84665a355a6883bbdbc8bf6a1c3197d1700c64295ed2a6e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Biosynthesis</topic><topic>Digestive system</topic><topic>diphthamidation</topic><topic>Drosophila</topic><topic>Gastrointestinal tract</topic><topic>Gene expression</topic><topic>Gene regulation</topic><topic>Hyperplasia</topic><topic>Hypertrophy</topic><topic>Insects</topic><topic>Intestine</topic><topic>Life span</topic><topic>Myc</topic><topic>Phenotypes</topic><topic>Ras</topic><topic>Ras protein</topic><topic>Stem cells</topic><topic>Translation</topic><topic>tumor</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tsuda‐Sakurai, Kayoko</creatorcontrib><creatorcontrib>Kimura, Masaki</creatorcontrib><creatorcontrib>Miura, Masayuki</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Genes to cells : devoted to molecular & cellular mechanisms</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tsuda‐Sakurai, Kayoko</au><au>Kimura, Masaki</au><au>Miura, Masayuki</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Diphthamide modification of eEF2 is required for gut tumor‐like hyperplasia induced by oncogenic Ras</atitle><jtitle>Genes to cells : devoted to molecular & cellular mechanisms</jtitle><addtitle>Genes Cells</addtitle><date>2020-02</date><risdate>2020</risdate><volume>25</volume><issue>2</issue><spage>76</spage><epage>85</epage><pages>76-85</pages><issn>1356-9597</issn><eissn>1365-2443</eissn><abstract>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 life span. 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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| subjects | Biosynthesis Digestive system diphthamidation Drosophila Gastrointestinal tract Gene expression Gene regulation Hyperplasia Hypertrophy Insects Intestine Life span Myc Phenotypes Ras Ras protein Stem cells Translation tumor |
| title | Diphthamide modification of eEF2 is required for gut tumor‐like hyperplasia induced by oncogenic Ras |
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