LATS suppresses mTORC1 activity to directly coordinate Hippo and mTORC1 pathways in growth control
The Hippo and mammalian target of rapamycin complex 1 (mTORC1) pathways are the two predominant growth-control pathways that dictate proper organ development. We therefore explored potential crosstalk between these two functionally relevant pathways to coordinate their growth-control functions. We f...
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| Published in | Nature cell biology Vol. 22; no. 2; pp. 246 - 256 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
London
Nature Publishing Group UK
01.02.2020
Nature Publishing Group |
| Subjects | |
| Online Access | Get full text |
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| Abstract | The Hippo and mammalian target of rapamycin complex 1 (mTORC1) pathways are the two predominant growth-control pathways that dictate proper organ development. We therefore explored potential crosstalk between these two functionally relevant pathways to coordinate their growth-control functions. We found that the LATS1 and LATS2 kinases, the core components of the Hippo pathway, phosphorylate S606 of Raptor, an essential component of mTORC1, to attenuate mTORC1 activation by impairing the interaction of Raptor with Rheb. The phosphomimetic Raptor-S606D knock-in mutant led to a reduction in cell size and proliferation. Compared with
Raptor
+/+
mice,
Raptor
D/D
knock-in mice exhibited smaller livers and hearts, and a significant inhibition of elevation in mTORC1 signalling induced by
Nf2
or
Lats1
and
Lats2
loss. Thus, our study reveals a direct link between the Hippo and mTORC1 pathways to fine-tune organ growth.
The Hippo and mTORC1 pathways regulate growth control for proper organ development. Here, Gan et al. find that the Hippo pathway kinases LATS1 and LATS2 phosphorylate the mTORC1 component Raptor to attenuate mTORC1 activation. |
|---|---|
| AbstractList | The Hippo and mammalian target of rapamycin complex 1 (mTORC1) pathways are the two predominant growth-control pathways that dictate proper organ development. We therefore explored potential crosstalk between these two functionally relevant pathways to coordinate their growth-control functions. We found that the LATS1 and LATS2 kinases, the core components of the Hippo pathway, phosphorylate S606 of Raptor, an essential component of mTORC1, to attenuate mTORC1 activation by impairing the interaction of Raptor with Rheb. The phosphomimetic Raptor-S606D knock-in mutant led to a reduction in cell size and proliferation. Compared with Raptor.sup.+/+ mice, Raptor.sup.D/D knock-in mice exhibited smaller livers and hearts, and a significant inhibition of elevation in mTORC1 signalling induced by Nf2 or Lats1 and Lats2 loss. Thus, our study reveals a direct link between the Hippo and mTORC1 pathways to fine-tune organ growth. The Hippo and mTORC1 pathways regulate growth control for proper organ development. Here, Gan et al. find that the Hippo pathway kinases LATS1 and LATS2 phosphorylate the mTORC1 component Raptor to attenuate mTORC1 activation. The Hippo and mammalian target of rapamycin complex 1 (mTORC1) pathways are the two predominant growth-control pathways that dictate proper organ development. We therefore explored potential crosstalk between these two functionally relevant pathways to coordinate their growth-control functions. We found that the LATS1 and LATS2 kinases, the core components of the Hippo pathway, phosphorylate S606 of Raptor, an essential component of mTORC1, to attenuate mTORC1 activation by impairing the interaction of Raptor with Rheb. The phosphomimetic Raptor-S606D knock-in mutant led to a reduction in cell size and proliferation. Compared with Raptor mice, Raptor knock-in mice exhibited smaller livers and hearts, and a significant inhibition of elevation in mTORC1 signalling induced by Nf2 or Lats1 and Lats2 loss. Thus, our study reveals a direct link between the Hippo and mTORC1 pathways to fine-tune organ growth. The Hippo and mammalian target of rapamycin complex 1 (mTORC1) pathways are the two predominant growth-control pathways that dictate proper organ development. We therefore explored potential crosstalk between these two functionally relevant pathways to coordinate their growth-control functions. We found that the LATS1 and LATS2 kinases, the core components of the Hippo pathway, phosphorylate S606 of Raptor, an essential component of mTORC1, to attenuate mTORC1 activation by impairing the interaction of Raptor with Rheb. The phosphomimetic Raptor-S606D knock-in mutant led to a reduction in cell size and proliferation. Compared with Raptor +/+ mice, Raptor D/D knock-in mice exhibited smaller livers and hearts, and a significant inhibition of elevation in mTORC1 signalling induced by Nf2 or Lats1 and Lats2 loss. Thus, our study reveals a direct link between the Hippo and mTORC1 pathways to fine-tune organ growth. The Hippo and mTORC1 pathways regulate growth control for proper organ development. Here, Gan et al. find that the Hippo pathway kinases LATS1 and LATS2 phosphorylate the mTORC1 component Raptor to attenuate mTORC1 activation. The Hippo and mammalian target of rapamycin complex 1 (mTORC1) pathways are the two predominant growth-control pathways that dictate proper organ development. We therefore explored potential crosstalk between these two functionally relevant pathways to coordinate their growth-control functions. We found that the LATS1 and LATS2 kinases, the core components of the Hippo pathway, phosphorylate S606 of Raptor, an essential component of mTORC1, to attenuate mTORC1 activation by impairing the interaction of Raptor with Rheb. The phosphomimetic Raptor-S606D knock-in mutant led to a reduction in cell size and proliferation. Compared with Raptor.sup.+/+ mice, Raptor.sup.D/D knock-in mice exhibited smaller livers and hearts, and a significant inhibition of elevation in mTORC1 signalling induced by Nf2 or Lats1 and Lats2 loss. Thus, our study reveals a direct link between the Hippo and mTORC1 pathways to fine-tune organ growth. The Hippo and mammalian target of rapamycin complex 1 (mTORC1) pathways are the two predominant growth-control pathways that dictate proper organ development. We therefore explored potential crosstalk between these two functionally relevant pathways to coordinate their growth-control functions. We found that the LATS1 and LATS2 kinases, the core components of the Hippo pathway, phosphorylate S606 of Raptor, an essential component of mTORC1, to attenuate mTORC1 activation by impairing the interaction of Raptor with Rheb. The phosphomimetic Raptor-S606D knock-in mutant led to a reduction in cell size and proliferation. Compared with Raptor+/+ mice, RaptorD/D knock-in mice exhibited smaller livers and hearts, and a significant inhibition of elevation in mTORC1 signalling induced by Nf2 or Lats1 and Lats2 loss. Thus, our study reveals a direct link between the Hippo and mTORC1 pathways to fine-tune organ growth.The Hippo and mammalian target of rapamycin complex 1 (mTORC1) pathways are the two predominant growth-control pathways that dictate proper organ development. We therefore explored potential crosstalk between these two functionally relevant pathways to coordinate their growth-control functions. We found that the LATS1 and LATS2 kinases, the core components of the Hippo pathway, phosphorylate S606 of Raptor, an essential component of mTORC1, to attenuate mTORC1 activation by impairing the interaction of Raptor with Rheb. The phosphomimetic Raptor-S606D knock-in mutant led to a reduction in cell size and proliferation. Compared with Raptor+/+ mice, RaptorD/D knock-in mice exhibited smaller livers and hearts, and a significant inhibition of elevation in mTORC1 signalling induced by Nf2 or Lats1 and Lats2 loss. Thus, our study reveals a direct link between the Hippo and mTORC1 pathways to fine-tune organ growth. The Hippo and mammalian target of rapamycin complex 1 (mTORC1) pathways are the two predominant growth-control pathways that dictate proper organ development. We therefore explored potential crosstalk between these two functionally relevant pathways to coordinate their growth-control functions. We found that the LATS1 and LATS2 kinases, the core components of the Hippo pathway, phosphorylate S606 of Raptor, an essential component of mTORC1, to attenuate mTORC1 activation by impairing the interaction of Raptor with Rheb. The phosphomimetic Raptor-S606D knock-in mutant led to a reduction in cell size and proliferation. Compared with Raptor+/+ mice, RaptorD/D knock-in mice exhibited smaller livers and hearts, and a significant inhibition of elevation in mTORC1 signalling induced by Nf2 or Lats1 and Lats2 loss. Thus, our study reveals a direct link between the Hippo and mTORC1 pathways to fine-tune organ growth.The Hippo and mTORC1 pathways regulate growth control for proper organ development. Here, Gan et al. find that the Hippo pathway kinases LATS1 and LATS2 phosphorylate the mTORC1 component Raptor to attenuate mTORC1 activation. The Hippo and mTORC1 pathways are the two predominant growth-control pathways that dictate proper organ development. We therefore explored a possible crosstalk between these two functional relevant pathways to coordinate their growth-control functions. We found that the LATS1/2 kinases, the core component of the Hippo pathway, phosphorylate Ser606 of Raptor, an essential component of mTORC1, to attenuate mTORC1 activation through impairing Raptor interaction with Rheb. The phosphomimetic Raptor-S606D knock-in mutant leads to a reduction in cell size and cell proliferation. Compared to Raptor +/+ mice, Raptor D/D knock-in mice exhibit smaller liver and heart, and a significant inhibition of Nf2 or Lats1/2 loss-induced elevation of mTORC1 signaling and liver size. Thus, our study reveals a direct link between the Hippo and mTORC1 pathways to fine-tune organ growth. |
| Audience | Academic |
| Author | Hu, Jia Liu, Jing Ganem, Neil J. Quinton, Ryan J. He, Zhigang Pandolfi, Pier Paolo Dai, Xiangpeng Xie, Jun Liu, Yuchen Gao, Guangping Wei, Wenyi Dai, Xiaoming Zhu, Junjie Asara, John M. Yang, Yingzi Wang, Chen Wang, Min Liu, Pengda Gan, Wenjian Yin, Shasha Guo, Jianping |
| AuthorAffiliation | 13 These authors contributed equally: Wenjian Gan, Xiaoming Dai 8 Cancer Research Institute, Beth Israel Deaconess Cancer Center, Department of Medicine and Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA 6 Department of Biochemistry and Biophysics, Lineberger Comprehensive Cancer Center, The University of North Carolina at Chapel Hill, NC 27599, USA 11 Departments of Biliary-Pancreatic Surgery, Affiliated Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, China 4 F.M. Kirby Neurobiology Center, Boston Children's Hospital and Department of Neurology, Harvard Medical School, 300 Longwood Avenue, Boston, MA 02115, USA 10 Division of Hematology and Oncology, Department of Medicine, Boston University School of Medicine, Boston, MA 02118, USA 2 Department of Biochemistry and Molecular Biology, Medical University of South Carolina, Charleston, SC 29425, USA 12 Departments of Urology, Affiliated |
| AuthorAffiliation_xml | – name: 4 F.M. Kirby Neurobiology Center, Boston Children's Hospital and Department of Neurology, Harvard Medical School, 300 Longwood Avenue, Boston, MA 02115, USA – name: 13 These authors contributed equally: Wenjian Gan, Xiaoming Dai – name: 1 Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA – name: 3 Li Weibo Institute for Rare Diseases Research and Horae Gene Therapy Center and Vector Core, University of Massachusetts Medical School, Worcester, MA 01605, USA – name: 7 Division of Signal Transduction, Beth Israel Deaconess Medical Center and Department of Medicine, Harvard Medical School, Boston, MA 02215, USA – name: 9 The Laboratory of Cancer Cell Biology, Department of Pharmacology and Experimental Therapeutics, Boston University School of Medicine, Boston, MA 02118, USA – name: 12 Departments of Urology, Affiliated Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, China – name: 5 Department of Developmental Biology, Harvard Stem Cell Institute, Harvard School of Dental Medicine, Boston, MA 02215, USA – name: 11 Departments of Biliary-Pancreatic Surgery, Affiliated Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, China – name: 2 Department of Biochemistry and Molecular Biology, Medical University of South Carolina, Charleston, SC 29425, USA – name: 8 Cancer Research Institute, Beth Israel Deaconess Cancer Center, Department of Medicine and Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA – name: 6 Department of Biochemistry and Biophysics, Lineberger Comprehensive Cancer Center, The University of North Carolina at Chapel Hill, NC 27599, USA – name: 10 Division of Hematology and Oncology, Department of Medicine, Boston University School of Medicine, Boston, MA 02118, USA |
| Author_xml | – sequence: 1 givenname: Wenjian orcidid: 0000-0001-7599-5020 surname: Gan fullname: Gan, Wenjian email: ganw@musc.edu organization: Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Department of Biochemistry and Molecular Biology, Medical University of South Carolina – sequence: 2 givenname: Xiaoming surname: Dai fullname: Dai, Xiaoming organization: Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School – sequence: 3 givenname: Xiangpeng surname: Dai fullname: Dai, Xiangpeng organization: Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School – sequence: 4 givenname: Jun orcidid: 0000-0001-9565-1567 surname: Xie fullname: Xie, Jun organization: Li Weibo Institute for Rare Diseases Research and Horae Gene Therapy Center and Vector Core, University of Massachusetts Medical School – sequence: 5 givenname: Shasha surname: Yin fullname: Yin, Shasha organization: Department of Biochemistry and Molecular Biology, Medical University of South Carolina – sequence: 6 givenname: Junjie surname: Zhu fullname: Zhu, Junjie organization: F.M. Kirby Neurobiology Center, Boston Children’s Hospital and Department of Neurology, Harvard Medical School – sequence: 7 givenname: Chen surname: Wang fullname: Wang, Chen organization: F.M. Kirby Neurobiology Center, Boston Children’s Hospital and Department of Neurology, Harvard Medical School – sequence: 8 givenname: Yuchen orcidid: 0000-0001-8922-9976 surname: Liu fullname: Liu, Yuchen organization: Department of Developmental Biology, Harvard Stem Cell Institute, Harvard School of Dental Medicine – sequence: 9 givenname: Jianping surname: Guo fullname: Guo, Jianping organization: Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School – sequence: 10 givenname: Min surname: Wang fullname: Wang, Min organization: Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Departments of Biliary-Pancreatic Surgery, Affiliated Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology – sequence: 11 givenname: Jing surname: Liu fullname: Liu, Jing organization: Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School – sequence: 12 givenname: Jia surname: Hu fullname: Hu, Jia organization: Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Departments of Urology, Affiliated Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology – sequence: 13 givenname: Ryan J. surname: Quinton fullname: Quinton, Ryan J. organization: The Laboratory of Cancer Cell Biology, Department of Pharmacology and Experimental Therapeutics, Boston University School of Medicine, Division of Hematology and Oncology, Department of Medicine, Boston University School of Medicine – sequence: 14 givenname: Neil J. surname: Ganem fullname: Ganem, Neil J. organization: The Laboratory of Cancer Cell Biology, Department of Pharmacology and Experimental Therapeutics, Boston University School of Medicine, Division of Hematology and Oncology, Department of Medicine, Boston University School of Medicine – sequence: 15 givenname: Pengda surname: Liu fullname: Liu, Pengda organization: Department of Biochemistry and Biophysics, Lineberger Comprehensive Cancer Center, The University of North Carolina at Chapel Hill – sequence: 16 givenname: John M. surname: Asara fullname: Asara, John M. organization: Division of Signal Transduction, Beth Israel Deaconess Medical Center and Department of Medicine, Harvard Medical School – sequence: 17 givenname: Pier Paolo orcidid: 0000-0002-5352-5295 surname: Pandolfi fullname: Pandolfi, Pier Paolo organization: Cancer Research Institute, Beth Israel Deaconess Cancer Center, Department of Medicine and Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School – sequence: 18 givenname: Yingzi orcidid: 0000-0003-3933-887X surname: Yang fullname: Yang, Yingzi organization: Department of Developmental Biology, Harvard Stem Cell Institute, Harvard School of Dental Medicine – sequence: 19 givenname: Zhigang orcidid: 0000-0001-6080-6880 surname: He fullname: He, Zhigang organization: F.M. Kirby Neurobiology Center, Boston Children’s Hospital and Department of Neurology, Harvard Medical School – sequence: 20 givenname: Guangping orcidid: 0000-0003-0097-9012 surname: Gao fullname: Gao, Guangping organization: Li Weibo Institute for Rare Diseases Research and Horae Gene Therapy Center and Vector Core, University of Massachusetts Medical School – sequence: 21 givenname: Wenyi orcidid: 0000-0003-0512-3811 surname: Wei fullname: Wei, Wenyi email: wwei2@bidmc.harvard.edu organization: Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/32015438$$D View this record in MEDLINE/PubMed |
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| ContentType | Journal Article |
| Copyright | The Author(s), under exclusive licence to Springer Nature Limited 2020 COPYRIGHT 2020 Nature Publishing Group 2020© The Author(s), under exclusive licence to Springer Nature Limited 2020 |
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| DOI | 10.1038/s41556-020-0463-6 |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 W.G. and W.W. designed the experiments. W.G. and X.M.D. performed the experiments with assistance from X.P.D., S.Y., J.G., M.W., J.L. J.H., R.J.Q., N. J. G. and P.L. J.M.A. performed the LC-MS/MS metabolomic profiling and mass spectrometry analysis of Raptor S606 phosphorylation. J.X., J.Z., C.W., Y.L., Y.Y, Z.H. and G.G helped to design and perform the experiments on AAV-mediated depletion of Nf2 and Lats1/2. W.W. and P.P.P supervised the study. W.G. and W.W. wrote the manuscript. All authors commented on the manuscript. Author contributions |
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| Snippet | The Hippo and mammalian target of rapamycin complex 1 (mTORC1) pathways are the two predominant growth-control pathways that dictate proper organ development.... The Hippo and mTORC1 pathways are the two predominant growth-control pathways that dictate proper organ development. We therefore explored a possible crosstalk... |
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| Title | LATS suppresses mTORC1 activity to directly coordinate Hippo and mTORC1 pathways in growth control |
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