Host CDK-1 and formin mediate microvillar effacement induced by enterohemorrhagic Escherichia coli
Enterohemorrhagic Escherichia coli (EHEC) induces changes to the intestinal cell cytoskeleton and formation of attaching and effacing lesions, characterized by the effacement of microvilli and then formation of actin pedestals to which the bacteria are tightly attached. Here, we use a Caenorhabditis...
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| Veröffentlicht in: | Nature communications 2021-01, Vol.12 (1), p.90-90, Article 90 |
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| creator | Huang, Cheng-Rung Kuo, Cheng-Ju Huang, Chih-Wen Chen, Yu-Ting Liu, Bang-Yu Lee, Chung-Ta Chen, Po-Lin Chang, Wen-Tsan Chen, Yun-Wen Lee, Tzer-Min Hsieh, Hui-Chen Chen, Chang-Shi |
| description | Enterohemorrhagic
Escherichia coli
(EHEC) induces changes to the intestinal cell cytoskeleton and formation of attaching and effacing lesions, characterized by the effacement of microvilli and then formation of actin pedestals to which the bacteria are tightly attached. Here, we use a
Caenorhabditis elegans
model of EHEC infection to show that microvillar effacement is mediated by a signalling pathway including mitotic cyclin-dependent kinase 1 (CDK1) and diaphanous-related formin 1 (CYK1). Similar observations are also made using EHEC-infected human intestinal cells in vitro. Our results support the use of
C. elegans
as a host model for studying attaching and effacing lesions in vivo, and reveal that the CDK1-formin signal axis is necessary for EHEC-induced microvillar effacement.
Enterohemorrhagic
Escherichia coli
(EHEC) induces formation of attaching and effacing lesions in the intestine. Here, Huang et al. use human intestinal cells and a
C. elegans
model of infection to show that the process is mediated by a host signaling pathway involving cyclin-dependent kinase CDK1 and formin CYK1. |
| doi_str_mv | 10.1038/s41467-020-20355-1 |
| format | Article |
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Escherichia coli
(EHEC) induces changes to the intestinal cell cytoskeleton and formation of attaching and effacing lesions, characterized by the effacement of microvilli and then formation of actin pedestals to which the bacteria are tightly attached. Here, we use a
Caenorhabditis elegans
model of EHEC infection to show that microvillar effacement is mediated by a signalling pathway including mitotic cyclin-dependent kinase 1 (CDK1) and diaphanous-related formin 1 (CYK1). Similar observations are also made using EHEC-infected human intestinal cells in vitro. Our results support the use of
C. elegans
as a host model for studying attaching and effacing lesions in vivo, and reveal that the CDK1-formin signal axis is necessary for EHEC-induced microvillar effacement.
Enterohemorrhagic
Escherichia coli
(EHEC) induces formation of attaching and effacing lesions in the intestine. Here, Huang et al. use human intestinal cells and a
C. elegans
model of infection to show that the process is mediated by a host signaling pathway involving cyclin-dependent kinase CDK1 and formin CYK1.</description><identifier>ISSN: 2041-1723</identifier><identifier>EISSN: 2041-1723</identifier><identifier>DOI: 10.1038/s41467-020-20355-1</identifier><identifier>PMID: 33397943</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13 ; 13/1 ; 13/31 ; 13/89 ; 14 ; 14/19 ; 14/28 ; 14/35 ; 631/326/41/2531 ; 631/326/421 ; 631/326/88 ; 631/80/128 ; 64 ; 64/11 ; Actin ; Actins - metabolism ; Animals ; Caco-2 Cells ; Caenorhabditis elegans - metabolism ; Caenorhabditis elegans - microbiology ; Caenorhabditis elegans - ultrastructure ; Caenorhabditis elegans Proteins - metabolism ; Carbohydrate Epimerases - metabolism ; Cell Cycle Proteins - metabolism ; Cyclin-dependent kinases ; Cytoskeleton ; E coli ; Enterohemorrhagic Escherichia coli - pathogenicity ; Enterohemorrhagic Escherichia coli - physiology ; Escherichia coli ; Formins ; Host-Pathogen Interactions ; Humanities and Social Sciences ; Humans ; Infections ; Intestine ; Intestines - microbiology ; Kinases ; Lesions ; Microvilli - metabolism ; Microvilli - microbiology ; Microvilli - pathology ; multidisciplinary ; Multidisciplinary Sciences ; Phosphorylation ; Phosphothreonine - metabolism ; Science ; Science & Technology ; Science & Technology - Other Topics ; Science (multidisciplinary) ; Signal transduction ; Signaling ; Virulence ; Worms</subject><ispartof>Nature communications, 2021-01, Vol.12 (1), p.90-90, Article 90</ispartof><rights>The Author(s) 2021</rights><rights>The Author(s) 2021. This work is published under https://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>true</woscitedreferencessubscribed><woscitedreferencescount>26</woscitedreferencescount><woscitedreferencesoriginalsourcerecordid>wos000665636000017</woscitedreferencesoriginalsourcerecordid><citedby>FETCH-LOGICAL-c540t-7d4c9f9c1b70dcd9339a41691f0b900fad555ee9b54769723fcfbcb202eeb1913</citedby><cites>FETCH-LOGICAL-c540t-7d4c9f9c1b70dcd9339a41691f0b900fad555ee9b54769723fcfbcb202eeb1913</cites><orcidid>0000-0002-8201-3635 ; 0000-0002-0912-4865 ; 0000-0002-2774-5948</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7782584/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7782584/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,728,781,785,865,886,2103,2115,27928,27929,39262,41124,42193,51580,53795,53797</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33397943$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Huang, Cheng-Rung</creatorcontrib><creatorcontrib>Kuo, Cheng-Ju</creatorcontrib><creatorcontrib>Huang, Chih-Wen</creatorcontrib><creatorcontrib>Chen, Yu-Ting</creatorcontrib><creatorcontrib>Liu, Bang-Yu</creatorcontrib><creatorcontrib>Lee, Chung-Ta</creatorcontrib><creatorcontrib>Chen, Po-Lin</creatorcontrib><creatorcontrib>Chang, Wen-Tsan</creatorcontrib><creatorcontrib>Chen, Yun-Wen</creatorcontrib><creatorcontrib>Lee, Tzer-Min</creatorcontrib><creatorcontrib>Hsieh, Hui-Chen</creatorcontrib><creatorcontrib>Chen, Chang-Shi</creatorcontrib><title>Host CDK-1 and formin mediate microvillar effacement induced by enterohemorrhagic Escherichia coli</title><title>Nature communications</title><addtitle>Nat Commun</addtitle><addtitle>NAT COMMUN</addtitle><addtitle>Nat Commun</addtitle><description>Enterohemorrhagic
Escherichia coli
(EHEC) induces changes to the intestinal cell cytoskeleton and formation of attaching and effacing lesions, characterized by the effacement of microvilli and then formation of actin pedestals to which the bacteria are tightly attached. Here, we use a
Caenorhabditis elegans
model of EHEC infection to show that microvillar effacement is mediated by a signalling pathway including mitotic cyclin-dependent kinase 1 (CDK1) and diaphanous-related formin 1 (CYK1). Similar observations are also made using EHEC-infected human intestinal cells in vitro. Our results support the use of
C. elegans
as a host model for studying attaching and effacing lesions in vivo, and reveal that the CDK1-formin signal axis is necessary for EHEC-induced microvillar effacement.
Enterohemorrhagic
Escherichia coli
(EHEC) induces formation of attaching and effacing lesions in the intestine. Here, Huang et al. use human intestinal cells and a
C. elegans
model of infection to show that the process is mediated by a host signaling pathway involving cyclin-dependent kinase CDK1 and formin CYK1.</description><subject>13</subject><subject>13/1</subject><subject>13/31</subject><subject>13/89</subject><subject>14</subject><subject>14/19</subject><subject>14/28</subject><subject>14/35</subject><subject>631/326/41/2531</subject><subject>631/326/421</subject><subject>631/326/88</subject><subject>631/80/128</subject><subject>64</subject><subject>64/11</subject><subject>Actin</subject><subject>Actins - metabolism</subject><subject>Animals</subject><subject>Caco-2 Cells</subject><subject>Caenorhabditis elegans - metabolism</subject><subject>Caenorhabditis elegans - microbiology</subject><subject>Caenorhabditis elegans - ultrastructure</subject><subject>Caenorhabditis elegans Proteins - metabolism</subject><subject>Carbohydrate Epimerases - metabolism</subject><subject>Cell Cycle Proteins - metabolism</subject><subject>Cyclin-dependent 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CDK-1 and formin mediate microvillar effacement induced by enterohemorrhagic Escherichia coli</title><author>Huang, Cheng-Rung ; Kuo, Cheng-Ju ; Huang, Chih-Wen ; Chen, Yu-Ting ; Liu, Bang-Yu ; Lee, Chung-Ta ; Chen, Po-Lin ; Chang, Wen-Tsan ; Chen, Yun-Wen ; Lee, Tzer-Min ; Hsieh, Hui-Chen ; Chen, Chang-Shi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c540t-7d4c9f9c1b70dcd9339a41691f0b900fad555ee9b54769723fcfbcb202eeb1913</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>13</topic><topic>13/1</topic><topic>13/31</topic><topic>13/89</topic><topic>14</topic><topic>14/19</topic><topic>14/28</topic><topic>14/35</topic><topic>631/326/41/2531</topic><topic>631/326/421</topic><topic>631/326/88</topic><topic>631/80/128</topic><topic>64</topic><topic>64/11</topic><topic>Actin</topic><topic>Actins - metabolism</topic><topic>Animals</topic><topic>Caco-2 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Chih-Wen</au><au>Chen, Yu-Ting</au><au>Liu, Bang-Yu</au><au>Lee, Chung-Ta</au><au>Chen, Po-Lin</au><au>Chang, Wen-Tsan</au><au>Chen, Yun-Wen</au><au>Lee, Tzer-Min</au><au>Hsieh, Hui-Chen</au><au>Chen, Chang-Shi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Host CDK-1 and formin mediate microvillar effacement induced by enterohemorrhagic Escherichia coli</atitle><jtitle>Nature communications</jtitle><stitle>Nat Commun</stitle><stitle>NAT COMMUN</stitle><addtitle>Nat Commun</addtitle><date>2021-01-04</date><risdate>2021</risdate><volume>12</volume><issue>1</issue><spage>90</spage><epage>90</epage><pages>90-90</pages><artnum>90</artnum><issn>2041-1723</issn><eissn>2041-1723</eissn><abstract>Enterohemorrhagic
Escherichia coli
(EHEC) induces changes to the intestinal cell cytoskeleton and formation of attaching and effacing lesions, characterized by the effacement of microvilli and then formation of actin pedestals to which the bacteria are tightly attached. Here, we use a
Caenorhabditis elegans
model of EHEC infection to show that microvillar effacement is mediated by a signalling pathway including mitotic cyclin-dependent kinase 1 (CDK1) and diaphanous-related formin 1 (CYK1). Similar observations are also made using EHEC-infected human intestinal cells in vitro. Our results support the use of
C. elegans
as a host model for studying attaching and effacing lesions in vivo, and reveal that the CDK1-formin signal axis is necessary for EHEC-induced microvillar effacement.
Enterohemorrhagic
Escherichia coli
(EHEC) induces formation of attaching and effacing lesions in the intestine. Here, Huang et al. use human intestinal cells and a
C. elegans
model of infection to show that the process is mediated by a host signaling pathway involving cyclin-dependent kinase CDK1 and formin CYK1.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>33397943</pmid><doi>10.1038/s41467-020-20355-1</doi><tpages>19</tpages><orcidid>https://orcid.org/0000-0002-8201-3635</orcidid><orcidid>https://orcid.org/0000-0002-0912-4865</orcidid><orcidid>https://orcid.org/0000-0002-2774-5948</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | Nature communications, 2021-01, Vol.12 (1), p.90-90, Article 90 |
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| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_7782584 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Springer Nature OA Free Journals; Nature Free; Web of Science - Science Citation Index Expanded - 2021<img src="https://exlibris-pub.s3.amazonaws.com/fromwos-v2.jpg" />; EZB-FREE-00999 freely available EZB journals; PubMed Central; Alma/SFX Local Collection |
| subjects | 13 13/1 13/31 13/89 14 14/19 14/28 14/35 631/326/41/2531 631/326/421 631/326/88 631/80/128 64 64/11 Actin Actins - metabolism Animals Caco-2 Cells Caenorhabditis elegans - metabolism Caenorhabditis elegans - microbiology Caenorhabditis elegans - ultrastructure Caenorhabditis elegans Proteins - metabolism Carbohydrate Epimerases - metabolism Cell Cycle Proteins - metabolism Cyclin-dependent kinases Cytoskeleton E coli Enterohemorrhagic Escherichia coli - pathogenicity Enterohemorrhagic Escherichia coli - physiology Escherichia coli Formins Host-Pathogen Interactions Humanities and Social Sciences Humans Infections Intestine Intestines - microbiology Kinases Lesions Microvilli - metabolism Microvilli - microbiology Microvilli - pathology multidisciplinary Multidisciplinary Sciences Phosphorylation Phosphothreonine - metabolism Science Science & Technology Science & Technology - Other Topics Science (multidisciplinary) Signal transduction Signaling Virulence Worms |
| title | Host CDK-1 and formin mediate microvillar effacement induced by enterohemorrhagic Escherichia coli |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-16T16%3A38%3A57IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Host%20CDK-1%20and%20formin%20mediate%20microvillar%20effacement%20induced%20by%20enterohemorrhagic%20Escherichia%20coli&rft.jtitle=Nature%20communications&rft.au=Huang,%20Cheng-Rung&rft.date=2021-01-04&rft.volume=12&rft.issue=1&rft.spage=90&rft.epage=90&rft.pages=90-90&rft.artnum=90&rft.issn=2041-1723&rft.eissn=2041-1723&rft_id=info:doi/10.1038/s41467-020-20355-1&rft_dat=%3Cproquest_pubme%3E2475398098%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2474984631&rft_id=info:pmid/33397943&rft_doaj_id=oai_doaj_org_article_f4b63533b7a9482ab5bd4e6b416ad6a9&rfr_iscdi=true |