LUBAC is essential for embryogenesis by preventing cell death and enabling haematopoiesis

The linear ubiquitin chain assembly complex (LUBAC) is required for optimal gene activation and prevention of cell death upon activation of immune receptors, including TNFR1 1 . Deficiency in the LUBAC components SHARPIN or HOIP in mice results in severe inflammation in adulthood or embryonic lethal...

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Published inNature (London) Vol. 557; no. 7703; pp. 112 - 117
Main Authors Peltzer, Nieves, Darding, Maurice, Montinaro, Antonella, Draber, Peter, Draberova, Helena, Kupka, Sebastian, Rieser, Eva, Fisher, Amanda, Hutchinson, Ciaran, Taraborrelli, Lucia, Hartwig, Torsten, Lafont, Elodie, Haas, Tobias L., Shimizu, Yutaka, Böiers, Charlotta, Sarr, Aida, Rickard, James, Alvarez-Diaz, Silvia, Ashworth, Michael T., Beal, Allison, Enver, Tariq, Bertin, John, Kaiser, William, Strasser, Andreas, Silke, John, Bouillet, Philippe, Walczak, Henning
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 01.05.2018
Nature Publishing Group
Subjects
13
13/1
13/2
13/21
13/31
13/51
14
14/1
14/34
14/63
38
38/91
42
45
631/136/2086
631/250/232/1473
631/80/458/582
631/80/82
64
64/60
82
82/1
Animals
Apoptosis
Assembly
Autoimmune diseases
Autoimmunity
Biochemistry
Carrier Proteins - chemistry
Carrier Proteins - genetics
Carrier Proteins - metabolism
Caspase
Caspase 8 - genetics
Caspase 8 - metabolism
Caspase-8
Cell activation
Cell death
Cell Death - genetics
Clonal deletion
Defects
Deregulation
Disease
Embryo Loss - genetics
Embryogenesis
Embryonic development
Embryonic Development - genetics
Embryonic growth stage
Embryos
Endothelial cells
Endothelial Cells - cytology
Endothelium
Female
Fetuses
Gestation
Health aspects
Hematopoiesis
Hematopoiesis - genetics
Humanities and Social Sciences
Inflammation
Kinases
Lethality
Letter
Ligases
Mice
Mice, Inbred C57BL
Mortality
multidisciplinary
Mutation
Phenotypes
Physiological aspects
Prevention
Protein Domains
Protein Kinases - genetics
Receptor-Interacting Protein Serine-Threonine Kinases - deficiency
Receptors
Receptors, Tumor Necrosis Factor, Type I - metabolism
Recruitment
Science
Science (multidisciplinary)
Signal Transduction
Trends
Tumor necrosis factor receptors
Tumor necrosis factor-TNF
Ubiquitin
Ubiquitin - metabolism
Ubiquitin-Protein Ligases - deficiency
Ubiquitin-Protein Ligases - genetics
Ubiquitin-Protein Ligases - metabolism
United States > US
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Abstract The linear ubiquitin chain assembly complex (LUBAC) is required for optimal gene activation and prevention of cell death upon activation of immune receptors, including TNFR1 1 . Deficiency in the LUBAC components SHARPIN or HOIP in mice results in severe inflammation in adulthood or embryonic lethality, respectively, owing to deregulation of TNFR1-mediated cell death 2 – 8 . In humans, deficiency in the third LUBAC component HOIL-1 causes autoimmunity and inflammatory disease, similar to HOIP deficiency, whereas HOIL-1 deficiency in mice was reported to cause no overt phenotype 9 – 11 . Here we show, by creating HOIL-1-deficient mice, that HOIL-1 is as essential for LUBAC function as HOIP, albeit for different reasons: whereas HOIP is the catalytically active component of LUBAC, HOIL-1 is required for LUBAC assembly, stability and optimal retention in the TNFR1 signalling complex, thereby preventing aberrant cell death. Both HOIL-1 and HOIP prevent embryonic lethality at mid-gestation by interfering with aberrant TNFR1-mediated endothelial cell death, which only partially depends on RIPK1 kinase activity. Co-deletion of caspase-8 with RIPK3 or MLKL prevents cell death in  Hoil-1 −/− (also known as Rbck1 −/− ) embryos, yet only the combined loss of caspase-8 with MLKL results in viable HOIL-1-deficient mice. Notably, triple-knockout Ripk3 −/− Casp8 −/− Hoil-1 −/− embryos die at late gestation owing to haematopoietic defects that are rescued by co-deletion of RIPK1 but not MLKL. Collectively, these results demonstrate that both HOIP and HOIL-1 are essential LUBAC components and are required for embryogenesis by preventing aberrant cell death. Furthermore, they reveal that when LUBAC and caspase-8 are absent, RIPK3 prevents RIPK1 from inducing embryonic lethality by causing defects in fetal haematopoiesis. The HOIL-1 component of the LUBAC ubiquitin ligase complex is required for LUBAC activity, which prevents lethality during embryogenesis by preventing aberrant TNFR1-mediated endothelial cell death and RIPK1-mediated defects in haematopoiesis.
AbstractList The Linear Ubiquitin chain Assembly Complex (LUBAC) is required for optimal gene activation and prevention of cell death upon activation of immune receptors, including TNFR1 1 . Deficiency in the LUBAC components SHARPIN or HOIP in mice results in severe inflammation in adulthood or embryonic lethality, respectively, due to deregulation of TNFR1-mediated cell death 2 – 8 . In humans, deficiency in the third LUBAC component, HOIL-1, causes autoimmunity and inflammatory disease, similar to HOIP deficiency, whereas HOIL-1 deficiency in mice was reported to cause no overt phenotype 9 – 11 . By creating HOIL-1-deficient mice, we here show that HOIL-1 is, however, as essential for LUBAC function as HOIP, albeit for different reasons: whereas HOIP is LUBAC’s catalytically active component, HOIL-1 is required for LUBAC assembly, stability and optimal retention in the TNFR1-signalling complex (TNFR1-SC), thereby preventing aberrant cell death. Both, HOIL-1 and HOIP prevent embryonic lethality at mid-gestation by interfering with aberrant TNFR1-mediated endothelial cell death, which only partially depends on RIPK1 kinase activity. Co-deletion of Caspase-8 with RIPK3 or MLKL prevents cell death in Hoil-1 -/- embryos, yet only combined loss of Caspase-8 with MLKL results in viable HOIL-1-deficient mice. Interestingly, Ripk3 -/- Caspase-8 -/- Hoil-1 -/- embryos die at late-gestation due to haematopoietic defects that are rescued by co-deletion of RIPK1 but not MLKL. Collectively, these results demonstrate that both, HOIP and HOIL-1 are essential LUBAC components and are required for embryogenesis by preventing aberrant cell death. Furthermore, they unveil that, when LUBAC and Caspase-8 are absent, RIPK3 prevents RIPK1 from inducing embryonic lethality by causing defects in foetal haematopoiesis.
The linear ubiquitin chain assembly complex (LUBAC) is required for optimal gene activation and prevention of cell death upon activation of immune receptors, including TNFR1.sup.1. Deficiency in the LUBAC components SHARPIN or HOIP in mice results in severe inflammation in adulthood or embryonic lethality, respectively, owing to deregulation of TNFR1-mediated cell death.sup.2-8. In humans, deficiency in the third LUBAC component HOIL-1 causes autoimmunity and inflammatory disease, similar to HOIP deficiency, whereas HOIL-1 deficiency in mice was reported to cause no overt phenotype.sup.9-11. Here we show, by creating HOIL-1-deficient mice, that HOIL-1 is as essential for LUBAC function as HOIP, albeit for different reasons: whereas HOIP is the catalytically active component of LUBAC, HOIL-1 is required for LUBAC assembly, stability and optimal retention in the TNFR1 signalling complex, thereby preventing aberrant cell death. Both HOIL-1 and HOIP prevent embryonic lethality at mid-gestation by interfering with aberrant TNFR1-mediated endothelial cell death, which only partially depends on RIPK1 kinase activity. Co-deletion of caspase-8 with RIPK3 or MLKL prevents cell death in Hoil-1.sup.-/- (also known as Rbck1.sup.-/-) embryos, yet only the combined loss of caspase-8 with MLKL results in viable HOIL-1-deficient mice. Notably, triple-knockout Ripk3.sup.-/-Casp8.sup.-/-Hoil-1.sup.-/- embryos die at late gestation owing to haematopoietic defects that are rescued by co-deletion of RIPK1 but not MLKL. Collectively, these results demonstrate that both HOIP and HOIL-1 are essential LUBAC components and are required for embryogenesis by preventing aberrant cell death. Furthermore, they reveal that when LUBAC and caspase-8 are absent, RIPK3 prevents RIPK1 from inducing embryonic lethality by causing defects in fetal haematopoiesis.The HOIL-1 component of the LUBAC ubiquitin ligase complex is required for LUBAC activity, which prevents lethality during embryogenesis by preventing aberrant TNFR1-mediated endothelial cell death and RIPK1-mediated defects in haematopoiesis.
The linear ubiquitin chain assembly complex (LUBAC) is required for optimal gene activation and prevention of cell death upon activation of immune receptors, including TNFR1.sup.1. Deficiency in the LUBAC components SHARPIN or HOIP in mice results in severe inflammation in adulthood or embryonic lethality, respectively, owing to deregulation of TNFR1-mediated cell death.sup.2-8. In humans, deficiency in the third LUBAC component HOIL-1 causes autoimmunity and inflammatory disease, similar to HOIP deficiency, whereas HOIL-1 deficiency in mice was reported to cause no overt phenotype.sup.9-11. Here we show, by creating HOIL-1-deficient mice, that HOIL-1 is as essential for LUBAC function as HOIP, albeit for different reasons: whereas HOIP is the catalytically active component of LUBAC, HOIL-1 is required for LUBAC assembly, stability and optimal retention in the TNFR1 signalling complex, thereby preventing aberrant cell death. Both HOIL-1 and HOIP prevent embryonic lethality at mid-gestation by interfering with aberrant TNFR1-mediated endothelial cell death, which only partially depends on RIPK1 kinase activity. Co-deletion of caspase-8 with RIPK3 or MLKL prevents cell death in Hoil-1.sup.-/- (also known as Rbck1.sup.-/-) embryos, yet only the combined loss of caspase-8 with MLKL results in viable HOIL-1-deficient mice. Notably, triple-knockout Ripk3.sup.-/-Casp8.sup.-/-Hoil-1.sup.-/- embryos die at late gestation owing to haematopoietic defects that are rescued by co-deletion of RIPK1 but not MLKL. Collectively, these results demonstrate that both HOIP and HOIL-1 are essential LUBAC components and are required for embryogenesis by preventing aberrant cell death. Furthermore, they reveal that when LUBAC and caspase-8 are absent, RIPK3 prevents RIPK1 from inducing embryonic lethality by causing defects in fetal haematopoiesis.
The linear ubiquitin chain assembly complex (LUBAC) is required for optimal gene activation and prevention of cell death upon activation of immune receptors, including TNFR11. Deficiency in the LUBAC components SHARPIN or HOIP in mice results in severe inflammation in adulthood or embryonic lethality, respectively, owing to deregulation of TNFR1-mediated cell death2-8. In humans, deficiency in the third LUBAC component HOIL-1 causes autoimmunity and inflammatory disease, similar to HOIP deficiency, whereas HOIL-1 deficiency in mice was reported to cause no overt phenotype9-11. Here we show, by creating HOIL-1-deficient mice, that HOIL-1 is as essential for LUBAC function as HOIP, albeit for different reasons: whereas HOIP is the catalytically active component of LUBAC, HOIL-1 is required for LUBAC assembly, stability and optimal retention in the TNFR1 signalling complex, thereby preventing aberrant cell death. Both HOIL-1 and HOIP prevent embryonic lethality at mid-gestation by interfering with aberrant TNFR1-mediated endothelial cell death, which only partially depends on RIPK1 kinase activity. Co-deletion of caspase-8 with RIPK3 or MLKL prevents cell death in Hoil-1-/- (also known as Rbck1-/-) embryos, yet only the combined loss of caspase-8 with MLKL results in viable HOIL-1-deficient mice. Notably, triple-knockout Ripk3-/-Casp8-/-Hoil-1-/- embryos die at late gestation owing to haematopoietic defects that are rescued by co-deletion of RIPK1 but not MLKL. Collectively, these results demonstrate that both HOIP and HOIL-1 are essential LUBAC components and are required for embryogenesis by preventing aberrant cell death. Furthermore, they reveal that when LUBAC and caspase-8 are absent, RIPK3 prevents RIPK1 from inducing embryonic lethality by causing defects in fetal haematopoiesis.
The linear ubiquitin chain assembly complex (LUBAC) is required for optimal gene activation and prevention of cell death upon activation of immune receptors, including TNFR1 . Deficiency in the LUBAC components SHARPIN or HOIP in mice results in severe inflammation in adulthood or embryonic lethality, respectively, owing to deregulation of TNFR1-mediated cell death . In humans, deficiency in the third LUBAC component HOIL-1 causes autoimmunity and inflammatory disease, similar to HOIP deficiency, whereas HOIL-1 deficiency in mice was reported to cause no overt phenotype . Here we show, by creating HOIL-1-deficient mice, that HOIL-1 is as essential for LUBAC function as HOIP, albeit for different reasons: whereas HOIP is the catalytically active component of LUBAC, HOIL-1 is required for LUBAC assembly, stability and optimal retention in the TNFR1 signalling complex, thereby preventing aberrant cell death. Both HOIL-1 and HOIP prevent embryonic lethality at mid-gestation by interfering with aberrant TNFR1-mediated endothelial cell death, which only partially depends on RIPK1 kinase activity. Co-deletion of caspase-8 with RIPK3 or MLKL prevents cell death in Hoil-1 (also known as Rbck1 ) embryos, yet only the combined loss of caspase-8 with MLKL results in viable HOIL-1-deficient mice. Notably, triple-knockout Ripk3 Casp8 Hoil-1 embryos die at late gestation owing to haematopoietic defects that are rescued by co-deletion of RIPK1 but not MLKL. Collectively, these results demonstrate that both HOIP and HOIL-1 are essential LUBAC components and are required for embryogenesis by preventing aberrant cell death. Furthermore, they reveal that when LUBAC and caspase-8 are absent, RIPK3 prevents RIPK1 from inducing embryonic lethality by causing defects in fetal haematopoiesis.
The linear ubiquitin chain assembly complex (LUBAC) is required for optimal gene activation and prevention of cell death upon activation of immune receptors, including TNFR1 1 . Deficiency in the LUBAC components SHARPIN or HOIP in mice results in severe inflammation in adulthood or embryonic lethality, respectively, owing to deregulation of TNFR1-mediated cell death 2 – 8 . In humans, deficiency in the third LUBAC component HOIL-1 causes autoimmunity and inflammatory disease, similar to HOIP deficiency, whereas HOIL-1 deficiency in mice was reported to cause no overt phenotype 9 – 11 . Here we show, by creating HOIL-1-deficient mice, that HOIL-1 is as essential for LUBAC function as HOIP, albeit for different reasons: whereas HOIP is the catalytically active component of LUBAC, HOIL-1 is required for LUBAC assembly, stability and optimal retention in the TNFR1 signalling complex, thereby preventing aberrant cell death. Both HOIL-1 and HOIP prevent embryonic lethality at mid-gestation by interfering with aberrant TNFR1-mediated endothelial cell death, which only partially depends on RIPK1 kinase activity. Co-deletion of caspase-8 with RIPK3 or MLKL prevents cell death in  Hoil-1 −/− (also known as Rbck1 −/− ) embryos, yet only the combined loss of caspase-8 with MLKL results in viable HOIL-1-deficient mice. Notably, triple-knockout Ripk3 −/− Casp8 −/− Hoil-1 −/− embryos die at late gestation owing to haematopoietic defects that are rescued by co-deletion of RIPK1 but not MLKL. Collectively, these results demonstrate that both HOIP and HOIL-1 are essential LUBAC components and are required for embryogenesis by preventing aberrant cell death. Furthermore, they reveal that when LUBAC and caspase-8 are absent, RIPK3 prevents RIPK1 from inducing embryonic lethality by causing defects in fetal haematopoiesis. The HOIL-1 component of the LUBAC ubiquitin ligase complex is required for LUBAC activity, which prevents lethality during embryogenesis by preventing aberrant TNFR1-mediated endothelial cell death and RIPK1-mediated defects in haematopoiesis.
Audience Academic
Author Strasser, Andreas
Kaiser, William
Kupka, Sebastian
Darding, Maurice
Draber, Peter
Böiers, Charlotta
Beal, Allison
Taraborrelli, Lucia
Ashworth, Michael T.
Peltzer, Nieves
Montinaro, Antonella
Lafont, Elodie
Fisher, Amanda
Hutchinson, Ciaran
Walczak, Henning
Alvarez-Diaz, Silvia
Bouillet, Philippe
Sarr, Aida
Hartwig, Torsten
Rieser, Eva
Bertin, John
Draberova, Helena
Shimizu, Yutaka
Haas, Tobias L.
Silke, John
Rickard, James
Enver, Tariq
AuthorAffiliation 5 The Walter and Eliza Hall Institute of Medical Research, 1G Royal Parade, Parkville, Victoria 3052, Australia
2 University of Texas Health Science Center, 7703 Floyd Curl Drive, San Antonio, TX 78229, USA
1 UCL Cancer Institute, University College London, 72 Huntley Street, London WC1E 6DD, UK
3 UCL Great Ormond Street Institute of Child Health, 30 Guilford St, London, UK
4 Institute of General Pathology, Università Cattolica del Sacro Cuore, 00168, Rome, Italy
6 Pattern Recognition Receptor Discovery Performance Unit, Immuno-Inflammation Therapeutic Area, GlaxoSmithKline, Collegeville, Pennsylvania, USA
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– name: 6 Pattern Recognition Receptor Discovery Performance Unit, Immuno-Inflammation Therapeutic Area, GlaxoSmithKline, Collegeville, Pennsylvania, USA
– name: 2 University of Texas Health Science Center, 7703 Floyd Curl Drive, San Antonio, TX 78229, USA
– name: 1 UCL Cancer Institute, University College London, 72 Huntley Street, London WC1E 6DD, UK
– name: 4 Institute of General Pathology, Università Cattolica del Sacro Cuore, 00168, Rome, Italy
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  organization: UCL Cancer Institute, University College London
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  organization: UCL Cancer Institute, University College London
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  organization: University of Texas Health Science Center
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  organization: UCL Cancer Institute, University College London
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  organization: UCL Cancer Institute, University College London
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  surname: Lafont
  fullname: Lafont, Elodie
  organization: UCL Cancer Institute, University College London
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  givenname: Yutaka
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  organization: UCL Cancer Institute, University College London
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  givenname: Charlotta
  surname: Böiers
  fullname: Böiers, Charlotta
  organization: UCL Cancer Institute, University College London
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  givenname: Aida
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  organization: UCL Cancer Institute, University College London
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  givenname: James
  surname: Rickard
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  organization: The Walter and Eliza Hall Institute of Medical Research, Department of Medical Biology, The University of Melbourne
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  givenname: Silvia
  surname: Alvarez-Diaz
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  organization: The Walter and Eliza Hall Institute of Medical Research, Department of Medical Biology, The University of Melbourne
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  givenname: Michael T.
  surname: Ashworth
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  organization: UCL Great Ormond Street Institute of Child Health
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  surname: Beal
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  organization: Pattern Recognition Receptor Discovery Performance Unit, Immuno-Inflammation Therapeutic Area, GlaxoSmithKline
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  organization: UCL Cancer Institute, University College London
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  surname: Bertin
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  organization: Pattern Recognition Receptor Discovery Performance Unit, Immuno-Inflammation Therapeutic Area, GlaxoSmithKline
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  surname: Kaiser
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  organization: University of Texas Health Science Center
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  surname: Strasser
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  organization: The Walter and Eliza Hall Institute of Medical Research, Department of Medical Biology, The University of Melbourne
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  givenname: John
  surname: Silke
  fullname: Silke, John
  organization: The Walter and Eliza Hall Institute of Medical Research, Department of Medical Biology, The University of Melbourne
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  givenname: Philippe
  surname: Bouillet
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  givenname: Henning
  surname: Walczak
  fullname: Walczak, Henning
  email: h.walczak@ucl.ac.uk
  organization: UCL Cancer Institute, University College London
BackLink https://www.ncbi.nlm.nih.gov/pubmed/29695863$$D View this record in MEDLINE/PubMed
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Snippet The linear ubiquitin chain assembly complex (LUBAC) is required for optimal gene activation and prevention of cell death upon activation of immune receptors,...
The Linear Ubiquitin chain Assembly Complex (LUBAC) is required for optimal gene activation and prevention of cell death upon activation of immune receptors,...
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SubjectTerms 13
13/1
13/2
13/21
13/31
13/51
14
14/1
14/34
14/63
38
38/91
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631/136/2086
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631/80/458/582
631/80/82
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82/1
Animals
Apoptosis
Assembly
Autoimmune diseases
Autoimmunity
Biochemistry
Carrier Proteins - chemistry
Carrier Proteins - genetics
Carrier Proteins - metabolism
Caspase
Caspase 8 - genetics
Caspase 8 - metabolism
Caspase-8
Cell activation
Cell death
Cell Death - genetics
Clonal deletion
Defects
Deregulation
Disease
Embryo Loss - genetics
Embryogenesis
Embryonic development
Embryonic Development - genetics
Embryonic growth stage
Embryos
Endothelial cells
Endothelial Cells - cytology
Endothelium
Female
Fetuses
Gestation
Health aspects
Hematopoiesis
Hematopoiesis - genetics
Humanities and Social Sciences
Inflammation
Kinases
Lethality
Letter
Ligases
Mice
Mice, Inbred C57BL
Mortality
multidisciplinary
Mutation
Phenotypes
Physiological aspects
Prevention
Protein Domains
Protein Kinases - genetics
Receptor-Interacting Protein Serine-Threonine Kinases - deficiency
Receptors
Receptors, Tumor Necrosis Factor, Type I - metabolism
Recruitment
Science
Science (multidisciplinary)
Signal Transduction
Trends
Tumor necrosis factor receptors
Tumor necrosis factor-TNF
Ubiquitin
Ubiquitin - metabolism
Ubiquitin-Protein Ligases - deficiency
Ubiquitin-Protein Ligases - genetics
Ubiquitin-Protein Ligases - metabolism
Title LUBAC is essential for embryogenesis by preventing cell death and enabling haematopoiesis
URI https://link.springer.com/article/10.1038/s41586-018-0064-8
https://www.ncbi.nlm.nih.gov/pubmed/29695863
https://www.proquest.com/docview/2057263543
https://search.proquest.com/docview/2031415873
https://pubmed.ncbi.nlm.nih.gov/PMC5947819
Volume 557
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