Mouse Nuclear Myosin I Knock-Out Shows Interchangeability and Redundancy of Myosin Isoforms in the Cell Nucleus

• DOI: 10.1371/journal.pone.0061406
• Publication Date: 2013-04-11T21:12:07Z
• Authors: Tomáš Venit; Rastislav Dzijak; Alžběta Kalendová; Michal Kahle; Jana Rohožková; Volker Schmidt; Thomas Rülicke; Birgit Rathkolb; Wolfgang Hans; Alexander Bohla; Oliver Eickelberg; Tobias Stoeger; Eckhard Wolf; Ali Önder Yildirim; Valérie Gailus-Du...; Helmut Fuchs; Martin Hrabě de A...; Pavel Hozák
• Keywords: Transcription

Nuclear myosin I (NM1) is a nuclear isoform of the well-known "cytoplasmic" Myosin 1c protein (Myo1c). Located on 11(th) chromosome in mice, NM1 results from an alternative start transcription Myo1c gene adding extra 16 amino acids at N-terminus. Previous studies revealed its roles RNA Polymerase and II transcription, chromatin remodeling, chromosomal movements. Its localization signal localized middle molecule therefore directs both isoforms to nucleus.In order trace specific functions isoform, we generated mice lacking codon without affecting cytoplasmic protein. Mutant were analyzed comprehensive phenotypic screen cooperation with German Mouse Clinic. Strikingly, no obvious phenotype related previously described has been observed. However, found minor changes bone mineral density number size red blood cells knock-out which are most probably not nucleus. In Myo1c/NM1 depleted U2OS cells, level Pol was restored by overexpression shRNA-resistant mouse Myo1c. Moreover, interacting II. The ratio between proteins similar nucleus deletion did cause any compensatory protein.We observed that can replace functions. Amount nearly equal does We suggest substitute each other processes.