PLoS One
Autor: | Elisa M. Nevalainen, Martina Serlachius, Attila Braun, Maria K. Vartiainen, Markus Moser, Leif C. Andersson, Pekka Lappalainen |
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Přispěvatelé: | Departments of Faculty of Veterinary Medicine, Institute of Biotechnology, Haartman Institute (-2014), Department of Pathology, Nuclear organization by actin |
Jazyk: | angličtina |
Rok vydání: | 2011 |
Předmět: |
Gene isoform
MECHANISM Blotting Western education lcsh:Medicine PROTEIN Cell Migration Biology 03 medical and health sciences Exon ACTIN MONOMERS MOTILITY Molecular Cell Biology Morphogenesis Animals YEAST Northern blot Cytoskeleton lcsh:Science Gene Actin 030304 developmental biology Mice Knockout 0303 health sciences Multidisciplinary Neuronal Morphology Reverse Transcriptase Polymerase Chain Reaction Tissue Extracts Microfilament Proteins 030302 biochemistry & molecular biology lcsh:R Brain Gene Expression Regulation Developmental Cell migration Blotting Northern Molecular biology Cellular Structures Cell biology MICE Organ Specificity Cellular Neuroscience Knockout mouse lcsh:Q Growth and Development Research Article Developmental Biology Neuroscience |
Zdroj: | PLoS ONE PLoS ONE, Vol 6, Iss 8, p e22894 (2011) |
Popis: | Twinfilins are evolutionarily conserved regulators of cytoskeletal dynamics. They inhibit actin polymerization by binding both actin monomers and filament barbed ends. Inactivation of the single twinfilin gene from budding yeast and fruit fly results in defects in endocytosis, cell migration, and organization of the cortical actin filament structures. Mammals express three twinfilin isoforms, of which twinfilin-1 and twinfilin-2a display largely overlapping expression patterns in non-muscle tissues of developing and adult mice. The expression of twinfilin-2b, which is generated through alternative promoter usage of the twinfilin-2 gene, is restricted to heart and skeletal muscles. However, the physiological functions of mammalian twinfilins have not been reported. As a first step towards understanding the function of twinfilin in vertebrates, we generated twinfilin-2a deficient mice by deleting exon 1 of the twinfilin-2 gene. Twinfilin-2a knockout mice developed normally to adulthood, were fertile, and did not display obvious morphological or behavioural abnormalities. Tissue anatomy and morphology in twinfilin-2a deficient mice was similar to that of wild-type littermates. These data suggest that twinfilin-2a plays a redundant role in cytoskeletal dynamics with the biochemically similar twinfilin-1, which is typically co-expressed in same tissues with twinfilin-2a. |
Databáze: | OpenAIRE |
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