Mlkl knockout mice demonstrate the indispensable role of Mlkl in necroptosis
Mixed lineage kinase domain-like protein （Mlkl） was recently found to interact with receptor interacting protein 3 （Rip3） and to be essential for tumor necrosis factor （TNF）-induced programmed necrosis （necroptosis） in cultured cell lines. We have generated Mlkl-deficient mice by transcription activ...
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| Published in | Cell research Vol. 23; no. 8; pp. 994 - 1006 |
|---|---|
| Main Authors | , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
London
Nature Publishing Group UK
01.08.2013
Nature Publishing Group |
| Subjects | |
| Online Access | Get full text |
| ISSN | 1001-0602 1748-7838 1748-7838 |
| DOI | 10.1038/cr.2013.91 |
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| Abstract | Mixed lineage kinase domain-like protein （Mlkl） was recently found to interact with receptor interacting protein 3 （Rip3） and to be essential for tumor necrosis factor （TNF）-induced programmed necrosis （necroptosis） in cultured cell lines. We have generated Mlkl-deficient mice by transcription activator-like effector nucleases （TALENs）-mediated gene disruption and found Mlkl to be dispensable for normal mouse development as well as immune cell develop- ment. Mlkl-deficient mouse embryonic fibroblasts （MEFs） and macrophages both showed resistance to necrotic but not apoptotic stimuli. Mlkl-deficient MEFs and macrophages were indistinguishable from wild-type cells in their abil- ity to activate NF-KB, ERK, JNK, and p38 in response to TNF and lipopolysaccharides （LPS）, respectively. Consis- tently, Mlkl-deficient macrophages and mice exhibited normal interleukin-lp （IL-1β）, IL-6, and TNF production after LPS treatment. Mlkl deficiency protects mice from cerulean-induced acute pancreatitis, a necrosis-related disease, but has no effect on polymicrobial septic shock-induced animal death. Our results provide genetic evidence for the role of Mlkl in necroptosis. |
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| AbstractList | Mixed lineage kinase domain-like protein (Mlkl) was recently found to interact with receptor interacting protein 3 (Rip3) and to be essential for tumor necrosis factor (TNF)-induced programmed necrosis (necroptosis) in cultured cell lines. We have generated Mlkl-deficient mice by transcription activator-like effector nucleases (TALENs)-mediated gene disruption and found Mlkl to be dispensable for normal mouse development as well as immune cell development. Mlkl-deficient mouse embryonic fibroblasts (MEFs) and macrophages both showed resistance to necrotic but not apoptotic stimuli. Mlkl-deficient MEFs and macrophages were indistinguishable from wild-type cells in their ability to activate NF-κB, ERK, JNK, and p38 in response to TNF and lipopolysaccharides (LPS), respectively. Consistently, Mlkl-deficient macrophages and mice exhibited normal interleukin-1β (IL-1β), IL-6, and TNF production after LPS treatment. Mlkl deficiency protects mice from cerulean-induced acute pancreatitis, a necrosis-related disease, but has no effect on polymicrobial septic shock-induced animal death. Our results provide genetic evidence for the role of Mlkl in necroptosis. Mixed lineage kinase domain-like protein (Mlkl) was recently found to interact with receptor interacting protein 3 (Rip3) and to be essential for tumor necrosis factor (TNF)-induced programmed necrosis (necroptosis) in cultured cell lines. We have generated Mlkl -deficient mice by transcription activator-like effector nucleases (TALENs)-mediated gene disruption and found Mlkl to be dispensable for normal mouse development as well as immune cell development. Mlkl -deficient mouse embryonic fibroblasts (MEFs) and macrophages both showed resistance to necrotic but not apoptotic stimuli. Mlkl -deficient MEFs and macrophages were indistinguishable from wild-type cells in their ability to activate NF-κB, ERK, JNK, and p38 in response to TNF and lipopolysaccharides (LPS), respectively. Consistently, Mlkl -deficient macrophages and mice exhibited normal interleukin-1β (IL-1β), IL-6, and TNF production after LPS treatment. Mlkl deficiency protects mice from cerulean-induced acute pancreatitis, a necrosis-related disease, but has no effect on polymicrobial septic shock-induced animal death. Our results provide genetic evidence for the role of Mlkl in necroptosis. Mixed lineage kinase domain-like protein （Mlkl） was recently found to interact with receptor interacting protein 3 （Rip3） and to be essential for tumor necrosis factor （TNF）-induced programmed necrosis （necroptosis） in cultured cell lines. We have generated Mlkl-deficient mice by transcription activator-like effector nucleases （TALENs）-mediated gene disruption and found Mlkl to be dispensable for normal mouse development as well as immune cell develop- ment. Mlkl-deficient mouse embryonic fibroblasts （MEFs） and macrophages both showed resistance to necrotic but not apoptotic stimuli. Mlkl-deficient MEFs and macrophages were indistinguishable from wild-type cells in their abil- ity to activate NF-KB, ERK, JNK, and p38 in response to TNF and lipopolysaccharides （LPS）, respectively. Consis- tently, Mlkl-deficient macrophages and mice exhibited normal interleukin-lp （IL-1β）, IL-6, and TNF production after LPS treatment. Mlkl deficiency protects mice from cerulean-induced acute pancreatitis, a necrosis-related disease, but has no effect on polymicrobial septic shock-induced animal death. Our results provide genetic evidence for the role of Mlkl in necroptosis. Mixed lineage kinase domain-like protein (Mlkl) was recently found to interact with receptor interacting protein 3 (Rip3) and to be essential for tumor necrosis factor (TNF)-induced programmed necrosis (necroptosis) in cultured cell lines. We have generated Mlkl-deficient mice by transcription activator-like effector nucleases (TALENs)-mediated gene disruption and found Mlkl to be dispensable for normal mouse development as well as immune cell development. Mlkl-deficient mouse embryonic fibroblasts (MEFs) and macrophages both showed resistance to necrotic but not apoptotic stimuli. Mlkl-deficient MEFs and macrophages were indistinguishable from wild-type cells in their ability to activate NF-κB, ERK, JNK, and p38 in response to TNF and lipopolysaccharides (LPS), respectively. Consistently, Mlkl-deficient macrophages and mice exhibited normal interleukin-1[beta] (IL-1[beta]), IL-6, and TNF production after LPS treatment. Mlkl deficiency protects mice from cerulean-induced acute pancreatitis, a necrosis-related disease, but has no effect on polymicrobial septic shock-induced animal death. Our results provide genetic evidence for the role of Mlkl in necroptosis. Mixed lineage kinase domain-like protein (Mlkl) was recently found to interact with receptor interacting protein 3 (Rip3) and to be essential for tumor necrosis factor (TNF)-induced programmed necrosis (necroptosis) in cultured cell lines. We have generated Mlkl-deficient mice by transcription activator-like effector nucleases (TALENs)-mediated gene disruption and found Mlkl to be dispensable for normal mouse development as well as immune cell development. Mlkl-deficient mouse embryonic fibroblasts (MEFs) and macrophages both showed resistance to necrotic but not apoptotic stimuli. Mlkl-deficient MEFs and macrophages were indistinguishable from wild-type cells in their ability to activate NF-κB, ERK, JNK, and p38 in response to TNF and lipopolysaccharides (LPS), respectively. Consistently, Mlkl-deficient macrophages and mice exhibited normal interleukin-1β (IL-1β), IL-6, and TNF production after LPS treatment. Mlkl deficiency protects mice from cerulean-induced acute pancreatitis, a necrosis-related disease, but has no effect on polymicrobial septic shock-induced animal death. Our results provide genetic evidence for the role of Mlkl in necroptosis.Mixed lineage kinase domain-like protein (Mlkl) was recently found to interact with receptor interacting protein 3 (Rip3) and to be essential for tumor necrosis factor (TNF)-induced programmed necrosis (necroptosis) in cultured cell lines. We have generated Mlkl-deficient mice by transcription activator-like effector nucleases (TALENs)-mediated gene disruption and found Mlkl to be dispensable for normal mouse development as well as immune cell development. Mlkl-deficient mouse embryonic fibroblasts (MEFs) and macrophages both showed resistance to necrotic but not apoptotic stimuli. Mlkl-deficient MEFs and macrophages were indistinguishable from wild-type cells in their ability to activate NF-κB, ERK, JNK, and p38 in response to TNF and lipopolysaccharides (LPS), respectively. Consistently, Mlkl-deficient macrophages and mice exhibited normal interleukin-1β (IL-1β), IL-6, and TNF production after LPS treatment. Mlkl deficiency protects mice from cerulean-induced acute pancreatitis, a necrosis-related disease, but has no effect on polymicrobial septic shock-induced animal death. Our results provide genetic evidence for the role of Mlkl in necroptosis. |
| Author | Jianfeng Wu Zhe Huang Junming Ren Zhirong Zhang Peng He Yangxin Li Jianhui Ma Wanze Chen Yingying Zhang Xiaojuan Zhou Zhentao Yang Su-Qin Wu Lanfen Chen Jiahuai Han |
| AuthorAffiliation | State Key Laboratory of Cellular Stress Biology and School of Life Sciences, Xiamen University, Xiamen, Fujian 361005, China |
| Author_xml | – sequence: 1 givenname: Jianfeng surname: Wu fullname: Wu, Jianfeng organization: State Key Laboratory of Cellular Stress Biology and School of Life Sciences, Xiamen University – sequence: 2 givenname: Zhe surname: Huang fullname: Huang, Zhe organization: State Key Laboratory of Cellular Stress Biology and School of Life Sciences, Xiamen University – sequence: 3 givenname: Junming surname: Ren fullname: Ren, Junming organization: State Key Laboratory of Cellular Stress Biology and School of Life Sciences, Xiamen University – sequence: 4 givenname: Zhirong surname: Zhang fullname: Zhang, Zhirong organization: State Key Laboratory of Cellular Stress Biology and School of Life Sciences, Xiamen University – sequence: 5 givenname: Peng surname: He fullname: He, Peng organization: State Key Laboratory of Cellular Stress Biology and School of Life Sciences, Xiamen University – sequence: 6 givenname: Yangxin surname: Li fullname: Li, Yangxin organization: State Key Laboratory of Cellular Stress Biology and School of Life Sciences, Xiamen University – sequence: 7 givenname: Jianhui surname: Ma fullname: Ma, Jianhui organization: State Key Laboratory of Cellular Stress Biology and School of Life Sciences, Xiamen University – sequence: 8 givenname: Wanze surname: Chen fullname: Chen, Wanze organization: State Key Laboratory of Cellular Stress Biology and School of Life Sciences, Xiamen University – sequence: 9 givenname: Yingying surname: Zhang fullname: Zhang, Yingying organization: State Key Laboratory of Cellular Stress Biology and School of Life Sciences, Xiamen University – sequence: 10 givenname: Xiaojuan surname: Zhou fullname: Zhou, Xiaojuan organization: State Key Laboratory of Cellular Stress Biology and School of Life Sciences, Xiamen University – sequence: 11 givenname: Zhentao surname: Yang fullname: Yang, Zhentao organization: State Key Laboratory of Cellular Stress Biology and School of Life Sciences, Xiamen University – sequence: 12 givenname: Su-Qin surname: Wu fullname: Wu, Su-Qin organization: State Key Laboratory of Cellular Stress Biology and School of Life Sciences, Xiamen University – sequence: 13 givenname: Lanfen surname: Chen fullname: Chen, Lanfen organization: State Key Laboratory of Cellular Stress Biology and School of Life Sciences, Xiamen University – sequence: 14 givenname: Jiahuai surname: Han fullname: Han, Jiahuai email: jhan@xmu.edu.cn, jhan@scripps.edu organization: State Key Laboratory of Cellular Stress Biology and School of Life Sciences, Xiamen University |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/23835476$$D View this record in MEDLINE/PubMed |
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| ContentType | Journal Article |
| Copyright | The Author(s) 2013 Copyright Nature Publishing Group Aug 2013 Copyright © 2013 Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences 2013 Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences |
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| DocumentTitleAlternate | Mlkl knockout mice demonstrate the indispensable role of Mlkl in necroptosis Characterization of Mlkl knockout mice |
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| Keywords | apoptosis Mlkl Rip3 TNF mice necroptosis |
| Language | English |
| License | https://creativecommons.org/licenses/by-nc-nd/3.0 This work is licensed under the Creative Commons Attribution-NonCommercial-No Derivative Works 3.0 Unported License. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-nd/3.0 |
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| Notes | Mlkl; necroptosis; apoptosis; TNF; Rip3; mice 31-1568/Q Mixed lineage kinase domain-like protein （Mlkl） was recently found to interact with receptor interacting protein 3 （Rip3） and to be essential for tumor necrosis factor （TNF）-induced programmed necrosis （necroptosis） in cultured cell lines. We have generated Mlkl-deficient mice by transcription activator-like effector nucleases （TALENs）-mediated gene disruption and found Mlkl to be dispensable for normal mouse development as well as immune cell develop- ment. Mlkl-deficient mouse embryonic fibroblasts （MEFs） and macrophages both showed resistance to necrotic but not apoptotic stimuli. Mlkl-deficient MEFs and macrophages were indistinguishable from wild-type cells in their abil- ity to activate NF-KB, ERK, JNK, and p38 in response to TNF and lipopolysaccharides （LPS）, respectively. Consis- tently, Mlkl-deficient macrophages and mice exhibited normal interleukin-lp （IL-1β）, IL-6, and TNF production after LPS treatment. Mlkl deficiency protects mice from cerulean-induced acute pancreatitis, a necrosis-related disease, but has no effect on polymicrobial septic shock-induced animal death. Our results provide genetic evidence for the role of Mlkl in necroptosis. ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 These three authors contributed equally to this work. |
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| PublicationTitle | Cell research |
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| PublicationYear | 2013 |
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| Snippet | Mixed lineage kinase domain-like protein （Mlkl） was recently found to interact with receptor interacting protein 3 （Rip3） and to be essential for tumor... Mixed lineage kinase domain-like protein (Mlkl) was recently found to interact with receptor interacting protein 3 (Rip3) and to be essential for tumor... |
| SourceID | pubmedcentral proquest pubmed crossref springer chongqing |
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| SubjectTerms | 631/45/127/1220 631/80/82/2344 631/80/86 Amino Acid Chloromethyl Ketones - pharmacology Animals Apoptosis Base Sequence Biomedical and Life Sciences Cell Biology Cell Line Interleukin-1beta - metabolism Interleukin-6 - metabolism Life Sciences Lipopolysaccharides - toxicity Macrophages - drug effects Macrophages - metabolism Male Mice Mice, Inbred C57BL Mice, Knockout Mitochondria - drug effects Mitochondria - metabolism Mitogen-Activated Protein Kinase Kinases - metabolism Necrosis NF-kappa B - metabolism NF-κB Original original-article Protein Kinases - deficiency Protein Kinases - genetics Protein Kinases - metabolism Receptor-Interacting Protein Serine-Threonine Kinases - deficiency Receptor-Interacting Protein Serine-Threonine Kinases - genetics Receptor-Interacting Protein Serine-Threonine Kinases - metabolism Signal Transduction - drug effects Tumor Necrosis Factor-alpha - pharmacology Tumor Necrosis Factors - metabolism 坏死性 基因敲除 小鼠 巨噬细胞 白细胞介素 肿瘤坏死因子 胚胎成纤维细胞 |
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| Title | Mlkl knockout mice demonstrate the indispensable role of Mlkl in necroptosis |
| URI | http://lib.cqvip.com/qk/85240X/201308/47078777.html https://link.springer.com/article/10.1038/cr.2013.91 https://www.ncbi.nlm.nih.gov/pubmed/23835476 https://www.proquest.com/docview/1416087537 https://www.proquest.com/docview/1417530337 https://pubmed.ncbi.nlm.nih.gov/PMC3731568 |
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