Randomization of left-right asymmetry due to loss of nodal cilia generating leftward flow of extraembryonic fluid in mice lacking KIF3B motor protein

Article Abstract:

A study was undertaken to examine the function and transport performance of the murine kinesin superfamily protein (KIF3) complex in vivo. KIF3B knockout mice were generated and the kif3B-/- mice manifested morphological abnormalities such as randomized left-right asymmetry observed in the heart tube looping. Results revealed that KIF3B-deficient mice demonstrated inadequate nodal cilia where the KIF3B was localized in wild-type embryos. Also, the wild-type nodal cilia were motile and produced a leftward flow of extraembryonic fluid in the nodal area.

Growth, Developmental biology, Symmetry (Biology), Embryology, Animal embryology, Nerve proteins, Nerve tissue proteins

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Targeted disruption of mouse conventional kinesin heavy chain, kif5B, results in abnormal perinuclear clustering of mitochondria

Article Abstract:

The microtubule-based motility of organelles in eukaryotic cells are controlled by kinesin superfamily proteins. In order to determine its biology, the mouse ubiquitous-type kinesin heavy chain (KHC) gene, kif5B was disrupted by homologous recombination. Its functional significance was then analyzed using a suppression system. Subsequent cell fractionations revealed a close association between KIF5B and the mitochondria. This suggests a possible role for the molecule in the transport of nonneuronal cells in the mitochondria.

Mitochondria, Cell physiology

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Charcot-Marie-Tooth disease type 2A caused by mutation in a microtubule motor KIF1Bbeta

Article Abstract:

Results reveal that Charcot-Marie-Tooth disease type 2A is a result of a loss-of-function mutation in the motor domain of the KIF1Bbeta gene, encoding the kinesin superfamily motor protein.

Japan, Statistical Data Included, Analysis, Physiological aspects, Gene mutations, Gene mutation, Peripheral nerve diseases, Peripheral nervous system diseases, Charcot-Marie-Tooth disease

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