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Related Concept Videos

In-vitro Mutagenesis01:16

In-vitro Mutagenesis

To learn more about the function of a gene, researchers can observe what happens when the gene is inactivated or “knocked out,” by creating genetically engineered knockout animals. Knockout mice have been particularly useful as models for human diseases such as cancer, Parkinson’s disease, and diabetes.

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Twinfilin-2a is dispensable for mouse development.

Elisa M Nevalainen1, Attila Braun, Maria K Vartiainen

  • 1Institute of Biotechnology, University of Helsinki, Helsinki, Finland.

Plos One
|August 31, 2011
PubMed
Summary

Twinfilin-2a knockout mice show no abnormalities, suggesting a redundant role in cytoskeletal dynamics. Twinfilin-2a likely compensates for twinfilin-1, as they are co-expressed in similar tissues.

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Area of Science:

  • Molecular Biology
  • Cell Biology
  • Biochemistry

Background:

  • Twinfilins are conserved proteins regulating actin dynamics by inhibiting polymerization.
  • In yeast and flies, twinfilin gene inactivation causes defects in endocytosis and cell migration.
  • Mammals have three twinfilin isoforms (twinfilin-1, -2a, -2b) with partially overlapping expression.

Purpose of the Study:

  • To investigate the physiological functions of mammalian twinfilins.
  • To understand the role of twinfilin-2a in vertebrate cytoskeletal dynamics.

Main Methods:

  • Generation of twinfilin-2a deficient mice via gene deletion.
  • Phenotypic analysis of knockout mice, including morphology, behavior, and fertility.

Main Results:

  • Twinfilin-2a knockout mice developed normally into adulthood.
  • No morphological or behavioral abnormalities were observed in the knockout mice.
  • Tissue anatomy and morphology were similar to wild-type littermates.

Conclusions:

  • Twinfilin-2a appears to have a redundant role in cytoskeletal regulation.
  • Twinfilin-1 likely compensates for the absence of twinfilin-2a due to co-expression and biochemical similarity.