Myosin 16 levels fluctuate during the cell cycle and are downregulated in response to DNA replication stress
Myosins comprise a highly conserved superfamily of eukaryotic actin‐dependent motor proteins implicated in a large repertoire of functions in both the cytoplasm and the nucleus. Class XVI myosin, MYO16, reveals expression in most somatic as well as meiotic cells with prominent localization in the nu...
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Published in | Cytoskeleton (Hoboken, N.J.) Vol. 70; no. 6; pp. 328 - 348 |
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Main Authors | , , |
Format | Journal Article |
Language | English |
Published |
United States
Blackwell Publishing Ltd
01.06.2013
Wiley Subscription Services, Inc |
Subjects | |
Online Access | Get full text |
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Summary: | Myosins comprise a highly conserved superfamily of eukaryotic actin‐dependent motor proteins implicated in a large repertoire of functions in both the cytoplasm and the nucleus. Class XVI myosin, MYO16, reveals expression in most somatic as well as meiotic cells with prominent localization in the nucleus, excepting the nucleolus; however, the role(s) of Myo16 in the nucleus remain unknown. In this report, we investigated Myo16 abundance during transit through the cell cycle. Immunolocalization, immunoblot, flow cytometric and quantitative RT‐PCR studies performed in Rat2 cells indicate that Myo16 mRNA and protein abundance are cell cycle regulated: in the unperturbed cell cycle, each rises to peak levels in late G1 and thereon through S‐phase and each decays as cells enter M‐phase. Notably, RNA interference‐induced Myo16 depletion results in altered cell cycle distribution as well as in large‐scale cell death. In response to DNA replication stress (impaired replication fork progression as a consequence of DNA damage, lack of sufficient deoxynucleotides, or inhibition of DNA polymerases), Myo16 protein shows substantial loss. Attenuation of replication stress (aphidicolin or hydroxyurea) is followed by a recovery of Myo16 expression and resumption of S‐phase progression. Collectively, these observations suggest that Myo16 may play a regulatory role in cell cycle progression. © 2013 Wiley Periodicals, Inc. |
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Bibliography: | Georgia Cancer Coalition ark:/67375/WNG-6JBWJ072-M ArticleID:CM21109 The Medical College of Georgia Research Institute istex:9BB8BD1928704885155B1D0669C59919E4400133 Monitoring Editor: Pekka Lappalainen ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 1949-3584 1949-3592 |
DOI: | 10.1002/cm.21109 |