Attenuated palmitoylation of serotonin receptor 5-HT1A affects receptor function and contributes to depression-like behaviors
The serotonergic system and in particular serotonin 1A receptor (5-HT1AR) are implicated in major depressive disorder (MDD). Here we demonstrated that 5-HT1AR is palmitoylated in human and rodent brains, and identified ZDHHC21 as a major palmitoyl acyltransferase, whose depletion reduced palmitoylat...
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| Vydáno v: | Nature communications Ročník 10; číslo 1; s. 3924 - 14 |
|---|---|
| Hlavní autoři: | , , , , , , , , , , , , , , , , , , , , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | angličtina |
| Vydáno: |
London
Nature Publishing Group UK
02.09.2019
Nature Publishing Group Nature Portfolio |
| Témata: | |
| ISSN: | 2041-1723, 2041-1723 |
| On-line přístup: | Získat plný text |
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| Abstract | The serotonergic system and in particular serotonin 1A receptor (5-HT1AR) are implicated in major depressive disorder (MDD). Here we demonstrated that 5-HT1AR is palmitoylated in human and rodent brains, and identified ZDHHC21 as a major palmitoyl acyltransferase, whose depletion reduced palmitoylation and consequently signaling functions of 5-HT1AR. Two rodent models for depression-like behavior show reduced brain ZDHHC21 expression and attenuated 5-HT1AR palmitoylation. Moreover, selective knock-down of ZDHHC21 in the murine forebrain induced depression-like behavior. We also identified the microRNA miR-30e as a negative regulator of
Zdhhc21
expression. Through analysis of the post-mortem brain samples in individuals with MDD that died by suicide we find that miR-30e expression is increased, while ZDHHC21 expression, as well as palmitoylation of 5-HT1AR, are reduced within the prefrontal cortex. Our study suggests that downregulation of 5-HT1AR palmitoylation is a mechanism involved in depression, making the restoration of 5-HT1AR palmitoylation a promising clinical strategy for the treatment of MDD.
Palmitoylation is a post translational modification that regulates GPCR activity. Here the authors show that palmitoylation of 5-HT1AR by the palmitoyltransferase enzyme ZDHHC21 contributes to depression-like behaviour in rodents and might be implicated in major depressive disorder. |
|---|---|
| AbstractList | Palmitoylation is a post translational modification that regulates GPCR activity. Here the authors show that palmitoylation of 5-HT1AR by the palmitoyltransferase enzyme ZDHHC21 contributes to depression-like behaviour in rodents and might be implicated in major depressive disorder. The serotonergic system and in particular serotonin 1A receptor (5-HT1AR) are implicated in major depressive disorder (MDD). Here we demonstrated that 5-HT1AR is palmitoylated in human and rodent brains, and identified ZDHHC21 as a major palmitoyl acyltransferase, whose depletion reduced palmitoylation and consequently signaling functions of 5-HT1AR. Two rodent models for depression-like behavior show reduced brain ZDHHC21 expression and attenuated 5-HT1AR palmitoylation. Moreover, selective knock-down of ZDHHC21 in the murine forebrain induced depression-like behavior. We also identified the microRNA miR-30e as a negative regulator of Zdhhc21 expression. Through analysis of the post-mortem brain samples in individuals with MDD that died by suicide we find that miR-30e expression is increased, while ZDHHC21 expression, as well as palmitoylation of 5-HT1AR, are reduced within the prefrontal cortex. Our study suggests that downregulation of 5-HT1AR palmitoylation is a mechanism involved in depression, making the restoration of 5-HT1AR palmitoylation a promising clinical strategy for the treatment of MDD. Palmitoylation is a post translational modification that regulates GPCR activity. Here the authors show that palmitoylation of 5-HT1AR by the palmitoyltransferase enzyme ZDHHC21 contributes to depression-like behaviour in rodents and might be implicated in major depressive disorder. The serotonergic system and in particular serotonin 1A receptor (5-HT1AR) are implicated in major depressive disorder (MDD). Here we demonstrated that 5-HT1AR is palmitoylated in human and rodent brains, and identified ZDHHC21 as a major palmitoyl acyltransferase, whose depletion reduced palmitoylation and consequently signaling functions of 5-HT1AR. Two rodent models for depression-like behavior show reduced brain ZDHHC21 expression and attenuated 5-HT1AR palmitoylation. Moreover, selective knock-down of ZDHHC21 in the murine forebrain induced depression-like behavior. We also identified the microRNA miR-30e as a negative regulator of Zdhhc21 expression. Through analysis of the post-mortem brain samples in individuals with MDD that died by suicide we find that miR-30e expression is increased, while ZDHHC21 expression, as well as palmitoylation of 5-HT1AR, are reduced within the prefrontal cortex. Our study suggests that downregulation of 5-HT1AR palmitoylation is a mechanism involved in depression, making the restoration of 5-HT1AR palmitoylation a promising clinical strategy for the treatment of MDD. Palmitoylation is a post translational modification that regulates GPCR activity. Here the authors show that palmitoylation of 5-HT1AR by the palmitoyltransferase enzyme ZDHHC21 contributes to depression-like behaviour in rodents and might be implicated in major depressive disorder. The serotonergic system and in particular serotonin 1A receptor (5-HT1AR) are implicated in major depressive disorder (MDD). Here we demonstrated that 5-HT1AR is palmitoylated in human and rodent brains, and identified ZDHHC21 as a major palmitoyl acyltransferase, whose depletion reduced palmitoylation and consequently signaling functions of 5-HT1AR. Two rodent models for depression-like behavior show reduced brain ZDHHC21 expression and attenuated 5-HT1AR palmitoylation. Moreover, selective knock-down of ZDHHC21 in the murine forebrain induced depression-like behavior. We also identified the microRNA miR-30e as a negative regulator of Zdhhc21 expression. Through analysis of the post-mortem brain samples in individuals with MDD that died by suicide we find that miR-30e expression is increased, while ZDHHC21 expression, as well as palmitoylation of 5-HT1AR, are reduced within the prefrontal cortex. Our study suggests that downregulation of 5-HT1AR palmitoylation is a mechanism involved in depression, making the restoration of 5-HT1AR palmitoylation a promising clinical strategy for the treatment of MDD. The serotonergic system and in particular serotonin 1A receptor (5-HT1AR) are implicated in major depressive disorder (MDD). Here we demonstrated that 5-HT1AR is palmitoylated in human and rodent brains, and identified ZDHHC21 as a major palmitoyl acyltransferase, whose depletion reduced palmitoylation and consequently signaling functions of 5-HT1AR. Two rodent models for depression-like behavior show reduced brain ZDHHC21 expression and attenuated 5-HT1AR palmitoylation. Moreover, selective knock-down of ZDHHC21 in the murine forebrain induced depression-like behavior. We also identified the microRNA miR-30e as a negative regulator of Zdhhc21 expression. Through analysis of the post-mortem brain samples in individuals with MDD that died by suicide we find that miR-30e expression is increased, while ZDHHC21 expression, as well as palmitoylation of 5-HT1AR, are reduced within the prefrontal cortex. Our study suggests that downregulation of 5-HT1AR palmitoylation is a mechanism involved in depression, making the restoration of 5-HT1AR palmitoylation a promising clinical strategy for the treatment of MDD. The serotonergic system and in particular serotonin 1A receptor (5-HT1AR) are implicated in major depressive disorder (MDD). Here we demonstrated that 5-HT1AR is palmitoylated in human and rodent brains, and identified ZDHHC21 as a major palmitoyl acyltransferase, whose depletion reduced palmitoylation and consequently signaling functions of 5-HT1AR. Two rodent models for depression-like behavior show reduced brain ZDHHC21 expression and attenuated 5-HT1AR palmitoylation. Moreover, selective knock-down of ZDHHC21 in the murine forebrain induced depression-like behavior. We also identified the microRNA miR-30e as a negative regulator of Zdhhc21 expression. Through analysis of the post-mortem brain samples in individuals with MDD that died by suicide we find that miR-30e expression is increased, while ZDHHC21 expression, as well as palmitoylation of 5-HT1AR, are reduced within the prefrontal cortex. Our study suggests that downregulation of 5-HT1AR palmitoylation is a mechanism involved in depression, making the restoration of 5-HT1AR palmitoylation a promising clinical strategy for the treatment of MDD.The serotonergic system and in particular serotonin 1A receptor (5-HT1AR) are implicated in major depressive disorder (MDD). Here we demonstrated that 5-HT1AR is palmitoylated in human and rodent brains, and identified ZDHHC21 as a major palmitoyl acyltransferase, whose depletion reduced palmitoylation and consequently signaling functions of 5-HT1AR. Two rodent models for depression-like behavior show reduced brain ZDHHC21 expression and attenuated 5-HT1AR palmitoylation. Moreover, selective knock-down of ZDHHC21 in the murine forebrain induced depression-like behavior. We also identified the microRNA miR-30e as a negative regulator of Zdhhc21 expression. Through analysis of the post-mortem brain samples in individuals with MDD that died by suicide we find that miR-30e expression is increased, while ZDHHC21 expression, as well as palmitoylation of 5-HT1AR, are reduced within the prefrontal cortex. Our study suggests that downregulation of 5-HT1AR palmitoylation is a mechanism involved in depression, making the restoration of 5-HT1AR palmitoylation a promising clinical strategy for the treatment of MDD. The serotonergic system and in particular serotonin 1A receptor (5-HT1AR) are implicated in major depressive disorder (MDD). Here we demonstrated that 5-HT1AR is palmitoylated in human and rodent brains, and identified ZDHHC21 as a major palmitoyl acyltransferase, whose depletion reduced palmitoylation and consequently signaling functions of 5-HT1AR. Two rodent models for depression-like behavior show reduced brain ZDHHC21 expression and attenuated 5-HT1AR palmitoylation. Moreover, selective knock-down of ZDHHC21 in the murine forebrain induced depression-like behavior. We also identified the microRNA miR-30e as a negative regulator of Zdhhc21 expression. Through analysis of the post-mortem brain samples in individuals with MDD that died by suicide we find that miR-30e expression is increased, while ZDHHC21 expression, as well as palmitoylation of 5-HT1AR, are reduced within the prefrontal cortex. Our study suggests that downregulation of 5-HT1AR palmitoylation is a mechanism involved in depression, making the restoration of 5-HT1AR palmitoylation a promising clinical strategy for the treatment of MDD. |
| ArticleNumber | 3924 |
| Author | Papaleo, Francesco Scheggia, Diego Smyth, Ian Zeug, Andre Ilchibaeva, Tatiana Sigrist, Stephan Krzystyniak, Adam Hobuß, Lisa Bijata, Monika Ponimaskin, Evgeni Prasad, Sonal Kondaurova, Elena Gorinski, Nataliya Zareba-Koziol, Monika Fiedler, Jan Thum, Thomas Pandey, Ghanshyam Wlodarczyk, Jakub Bazovkina, Daria Kulikova, Elizabeth Kochlamazashvili, Gaga Abdel Galil, Dalia Richter, Diethelm W. Bang, Claudia Naumenko, Vladimir S. Dityatev, Alexander Wirth, Alexander Strekalova, Tatyana |
| Author_xml | – sequence: 1 givenname: Nataliya orcidid: 0000-0002-5606-7162 surname: Gorinski fullname: Gorinski, Nataliya organization: Cellular Neurophysiology, Hannover Medical School – sequence: 2 givenname: Monika surname: Bijata fullname: Bijata, Monika organization: Cellular Neurophysiology, Hannover Medical School, Cell Biophysics, Nencki Institute – sequence: 3 givenname: Sonal surname: Prasad fullname: Prasad, Sonal organization: Cellular Neurophysiology, Hannover Medical School – sequence: 4 givenname: Alexander surname: Wirth fullname: Wirth, Alexander organization: Cellular Neurophysiology, Hannover Medical School – sequence: 5 givenname: Dalia surname: Abdel Galil fullname: Abdel Galil, Dalia organization: Cellular Neurophysiology, Hannover Medical School – sequence: 6 givenname: Andre orcidid: 0000-0001-9858-5841 surname: Zeug fullname: Zeug, Andre organization: Cellular Neurophysiology, Hannover Medical School – sequence: 7 givenname: Daria surname: Bazovkina fullname: Bazovkina, Daria organization: Behavioural Neurogenomics, Institute of Cytology and Genetics – sequence: 8 givenname: Elena surname: Kondaurova fullname: Kondaurova, Elena organization: Behavioural Neurogenomics, Institute of Cytology and Genetics – sequence: 9 givenname: Elizabeth surname: Kulikova fullname: Kulikova, Elizabeth organization: Behavioural Neurogenomics, Institute of Cytology and Genetics – sequence: 10 givenname: Tatiana surname: Ilchibaeva fullname: Ilchibaeva, Tatiana organization: Behavioural Neurogenomics, Institute of Cytology and Genetics – sequence: 11 givenname: Monika orcidid: 0000-0003-3544-6259 surname: Zareba-Koziol fullname: Zareba-Koziol, Monika organization: Cell Biophysics, Nencki Institute – sequence: 12 givenname: Francesco orcidid: 0000-0002-6326-0657 surname: Papaleo fullname: Papaleo, Francesco organization: Neuroscience and Brain Technologies, Istituto Italiano di Tecnologia – sequence: 13 givenname: Diego orcidid: 0000-0003-2586-9717 surname: Scheggia fullname: Scheggia, Diego organization: Neuroscience and Brain Technologies, Istituto Italiano di Tecnologia – sequence: 14 givenname: Gaga surname: Kochlamazashvili fullname: Kochlamazashvili, Gaga organization: Neuroscience and Brain Technologies, Istituto Italiano di Tecnologia – sequence: 15 givenname: Alexander orcidid: 0000-0002-0472-0553 surname: Dityatev fullname: Dityatev, Alexander organization: Neuroscience and Brain Technologies, Istituto Italiano di Tecnologia, Molecular Neuroplasticity, DZNE – sequence: 16 givenname: Ian surname: Smyth fullname: Smyth, Ian organization: Anatomy & Developmental Biology, Monash University – sequence: 17 givenname: Adam surname: Krzystyniak fullname: Krzystyniak, Adam organization: Cell Biophysics, Nencki Institute – sequence: 18 givenname: Jakub surname: Wlodarczyk fullname: Wlodarczyk, Jakub organization: Cell Biophysics, Nencki Institute – sequence: 19 givenname: Diethelm W. surname: Richter fullname: Richter, Diethelm W. organization: Neuro and Sensory Physiology, University of Göttingen – sequence: 20 givenname: Tatyana surname: Strekalova fullname: Strekalova, Tatyana organization: Sechenov First Moscow State Medical University, Neuroscience, Maastricht University, Laboratory of Psychiatric Neurobiology and Institute of General Pathology and Pathophysiology, Sechenov First Moscow State Medical University – sequence: 21 givenname: Stephan surname: Sigrist fullname: Sigrist, Stephan organization: Institute of Biology, Free University Berlin – sequence: 22 givenname: Claudia surname: Bang fullname: Bang, Claudia organization: Institute of Molecular and Translational Therapeutic Strategies, Hannover Medical School – sequence: 23 givenname: Lisa surname: Hobuß fullname: Hobuß, Lisa organization: Institute of Molecular and Translational Therapeutic Strategies, Hannover Medical School – sequence: 24 givenname: Jan surname: Fiedler fullname: Fiedler, Jan organization: Institute of Molecular and Translational Therapeutic Strategies, Hannover Medical School – sequence: 25 givenname: Thomas orcidid: 0000-0003-4360-1511 surname: Thum fullname: Thum, Thomas organization: Institute of Molecular and Translational Therapeutic Strategies, Hannover Medical School – sequence: 26 givenname: Vladimir S. surname: Naumenko fullname: Naumenko, Vladimir S. email: naumenko2002@mail.ru organization: Behavioural Neurogenomics, Institute of Cytology and Genetics – sequence: 27 givenname: Ghanshyam surname: Pandey fullname: Pandey, Ghanshyam email: GPandey@psych.uic.edu organization: Department of Psychiatry, University of Illinois – sequence: 28 givenname: Evgeni orcidid: 0000-0002-4570-5130 surname: Ponimaskin fullname: Ponimaskin, Evgeni email: Ponimaskin.evgeni@mh-hannover.de organization: Cellular Neurophysiology, Hannover Medical School |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/31477731$$D View this record in MEDLINE/PubMed https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-161244$$DView record from Swedish Publication Index (Linköpings universitet) |
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| ContentType | Journal Article |
| Copyright | The Author(s) 2019 2019. This work is published under http://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. |
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| Snippet | The serotonergic system and in particular serotonin 1A receptor (5-HT1AR) are implicated in major depressive disorder (MDD). Here we demonstrated that 5-HT1AR... Palmitoylation is a post translational modification that regulates GPCR activity. Here the authors show that palmitoylation of 5-HT1AR by the... |
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| Title | Attenuated palmitoylation of serotonin receptor 5-HT1A affects receptor function and contributes to depression-like behaviors |
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