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Mouse Nuclear Myosin I Knock-Out Shows Interchangeability and Redundancy of Myosin Isoforms in the Cell Nucleus
BACKGROUND: Nuclear myosin I (NM1) is a nuclear isoform of the well-known “cytoplasmic” Myosin 1c protein (Myo1c). Located on the 11(th) chromosome in mice, NM1 results from an alternative start of transcription of the Myo1c gene adding an extra 16 amino acids at the N-terminus. Previous studies rev...
Autores principales: | , , , , , , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Public Library of Science
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3623870/ https://www.ncbi.nlm.nih.gov/pubmed/23593477 http://dx.doi.org/10.1371/journal.pone.0061406 |
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author | Venit, Tomáš Dzijak, Rastislav Kalendová, Alžběta Kahle, Michal Rohožková, Jana Schmidt, Volker Rülicke, Thomas Rathkolb, Birgit Hans, Wolfgang Bohla, Alexander Eickelberg, Oliver Stoeger, Tobias Wolf, Eckhard Yildirim, Ali Önder Gailus-Durner, Valérie Fuchs, Helmut de Angelis, Martin Hrabě Hozák, Pavel |
author_facet | Venit, Tomáš Dzijak, Rastislav Kalendová, Alžběta Kahle, Michal Rohožková, Jana Schmidt, Volker Rülicke, Thomas Rathkolb, Birgit Hans, Wolfgang Bohla, Alexander Eickelberg, Oliver Stoeger, Tobias Wolf, Eckhard Yildirim, Ali Önder Gailus-Durner, Valérie Fuchs, Helmut de Angelis, Martin Hrabě Hozák, Pavel |
author_sort | Venit, Tomáš |
collection | PubMed |
description | BACKGROUND: Nuclear myosin I (NM1) is a nuclear isoform of the well-known “cytoplasmic” Myosin 1c protein (Myo1c). Located on the 11(th) chromosome in mice, NM1 results from an alternative start of transcription of the Myo1c gene adding an extra 16 amino acids at the N-terminus. Previous studies revealed its roles in RNA Polymerase I and RNA Polymerase II transcription, chromatin remodeling, and chromosomal movements. Its nuclear localization signal is localized in the middle of the molecule and therefore directs both Myosin 1c isoforms to the nucleus. METHODOLOGY/PRINCIPAL FINDINGS: In order to trace specific functions of the NM1 isoform, we generated mice lacking the NM1 start codon without affecting the cytoplasmic Myo1c protein. Mutant mice were analyzed in a comprehensive phenotypic screen in cooperation with the German Mouse Clinic. Strikingly, no obvious phenotype related to previously described functions has been observed. However, we found minor changes in bone mineral density and the number and size of red blood cells in knock-out mice, which are most probably not related to previously described functions of NM1 in the nucleus. In Myo1c/NM1 depleted U2OS cells, the level of Pol I transcription was restored by overexpression of shRNA-resistant mouse Myo1c. Moreover, we found Myo1c interacting with Pol II. The ratio between Myo1c and NM1 proteins were similar in the nucleus and deletion of NM1 did not cause any compensatory overexpression of Myo1c protein. CONCLUSION/SIGNIFICANCE: We observed that Myo1c can replace NM1 in its nuclear functions. Amount of both proteins is nearly equal and NM1 knock-out does not cause any compensatory overexpression of Myo1c. We therefore suggest that both isoforms can substitute each other in nuclear processes. |
format | Online Article Text |
id | pubmed-3623870 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | Public Library of Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-36238702013-04-16 Mouse Nuclear Myosin I Knock-Out Shows Interchangeability and Redundancy of Myosin Isoforms in the Cell Nucleus Venit, Tomáš Dzijak, Rastislav Kalendová, Alžběta Kahle, Michal Rohožková, Jana Schmidt, Volker Rülicke, Thomas Rathkolb, Birgit Hans, Wolfgang Bohla, Alexander Eickelberg, Oliver Stoeger, Tobias Wolf, Eckhard Yildirim, Ali Önder Gailus-Durner, Valérie Fuchs, Helmut de Angelis, Martin Hrabě Hozák, Pavel PLoS One Research Article BACKGROUND: Nuclear myosin I (NM1) is a nuclear isoform of the well-known “cytoplasmic” Myosin 1c protein (Myo1c). Located on the 11(th) chromosome in mice, NM1 results from an alternative start of transcription of the Myo1c gene adding an extra 16 amino acids at the N-terminus. Previous studies revealed its roles in RNA Polymerase I and RNA Polymerase II transcription, chromatin remodeling, and chromosomal movements. Its nuclear localization signal is localized in the middle of the molecule and therefore directs both Myosin 1c isoforms to the nucleus. METHODOLOGY/PRINCIPAL FINDINGS: In order to trace specific functions of the NM1 isoform, we generated mice lacking the NM1 start codon without affecting the cytoplasmic Myo1c protein. Mutant mice were analyzed in a comprehensive phenotypic screen in cooperation with the German Mouse Clinic. Strikingly, no obvious phenotype related to previously described functions has been observed. However, we found minor changes in bone mineral density and the number and size of red blood cells in knock-out mice, which are most probably not related to previously described functions of NM1 in the nucleus. In Myo1c/NM1 depleted U2OS cells, the level of Pol I transcription was restored by overexpression of shRNA-resistant mouse Myo1c. Moreover, we found Myo1c interacting with Pol II. The ratio between Myo1c and NM1 proteins were similar in the nucleus and deletion of NM1 did not cause any compensatory overexpression of Myo1c protein. CONCLUSION/SIGNIFICANCE: We observed that Myo1c can replace NM1 in its nuclear functions. Amount of both proteins is nearly equal and NM1 knock-out does not cause any compensatory overexpression of Myo1c. We therefore suggest that both isoforms can substitute each other in nuclear processes. Public Library of Science 2013-04-11 /pmc/articles/PMC3623870/ /pubmed/23593477 http://dx.doi.org/10.1371/journal.pone.0061406 Text en © 2013 Venit et al http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited. |
spellingShingle | Research Article Venit, Tomáš Dzijak, Rastislav Kalendová, Alžběta Kahle, Michal Rohožková, Jana Schmidt, Volker Rülicke, Thomas Rathkolb, Birgit Hans, Wolfgang Bohla, Alexander Eickelberg, Oliver Stoeger, Tobias Wolf, Eckhard Yildirim, Ali Önder Gailus-Durner, Valérie Fuchs, Helmut de Angelis, Martin Hrabě Hozák, Pavel Mouse Nuclear Myosin I Knock-Out Shows Interchangeability and Redundancy of Myosin Isoforms in the Cell Nucleus |
title | Mouse Nuclear Myosin I Knock-Out Shows Interchangeability and Redundancy of Myosin Isoforms in the Cell Nucleus |
title_full | Mouse Nuclear Myosin I Knock-Out Shows Interchangeability and Redundancy of Myosin Isoforms in the Cell Nucleus |
title_fullStr | Mouse Nuclear Myosin I Knock-Out Shows Interchangeability and Redundancy of Myosin Isoforms in the Cell Nucleus |
title_full_unstemmed | Mouse Nuclear Myosin I Knock-Out Shows Interchangeability and Redundancy of Myosin Isoforms in the Cell Nucleus |
title_short | Mouse Nuclear Myosin I Knock-Out Shows Interchangeability and Redundancy of Myosin Isoforms in the Cell Nucleus |
title_sort | mouse nuclear myosin i knock-out shows interchangeability and redundancy of myosin isoforms in the cell nucleus |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3623870/ https://www.ncbi.nlm.nih.gov/pubmed/23593477 http://dx.doi.org/10.1371/journal.pone.0061406 |
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