Cited by 31Microtubule and mitosis dynamicsCellular transport and secretionGenetic and Kidney Cyst Diseases

Molecular motor KIF1C is not essential for mouse survival and motor-dependent retrograde Golgi apparatus-to-endoplasmic reticulum transport

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Nakajima, Kazuo, Takei, Yosuke, Tanaka, Yosuke, Nakagawa, Terunaga, Nakata, Takao, Noda, Yasuko, Setou, Mitsutoshi, Hirokawa, Nobutaka·2002·Molecular and Cellular Biology

Abstract

KIF1C is a new member of the kinesin superfamily of proteins (KIFs), which act as microtubule-based molecular motors involved in intracellular transport. We cloned full-length mouse kif1C cDNA, which turned out to have a high homology to a mitochondrial motor KIF1Balpha and to be expressed ubiquitously. To investigate the in vivo significance of KIF1C, we generated kif1C(-/-) mice by knocking in the beta-galactosidase gene into the motor domain of kif1C gene. On staining of LacZ, we detected its expression in the heart, liver, hippocampus, and cerebellum. Unexpectedly, kif1C(-/-) mice were viable and showed no obvious abnormalities. Because immunocytochemistry showed partial colocalization of KIF1C with the Golgi marker protein, we compared the organelle distribution in primary lung fibroblasts from kif1C(+/+) and kif1C(-/-) mice. We found that there was no significant difference in the distribution of the Golgi apparatus or in the transport from the Golgi apparatus to the endoplasmic reticulum (ER) facilitated by brefeldin A between the two cells. This retrograde membrane transport was further confirmed to be normal by time-lapse analysis. Consequently, KIF1C is dispensable for the motor-dependent retrograde transport from the Golgi apparatus to the ER.

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Crossref · 10.1128/mcb.22.3.866-873.2002

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  • Fibroblasts from mice lacking KIF1C did not appear to show a morphological Golgi defect.

    “Fibroblasts from mice lacking KIF1C did not appear to show a morphological Golgi defect (Nakajima et al., 2002), but such cells likely compensate by expressing other proteins at higher levels and this subtle phenotype may have been missed.”

    From The Rab6-regulated KIF1C kinesin motor domain contributes to Golgi organization (2015) · cites this paper as Nakajima et al., 2002

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Authors
Nakajima, K., Takei, Y., Tanaka, Y., Nakagawa, T., Nakata, T., Noda, Y., Setou, M., & Hirokawa, N.
Affiliations
The University of Tokyo (JP)
Corresponding author
Hirokawa, Nobutaka
Venue
Molecular and Cellular Biology
Published
2002-02-01
Volume
22
Issue
3
Pages
866-873
ISSN
  • 0270-7306 (ISSN-L)
  • 1098-5549
OpenAlex
W2107318521
Cited by
31
References
42
Citations by year
2026: 1 · 2022: 1 · 2019: 2 · 2018: 1 · 2017: 1 · 2016: 1 · 2015: 1 · 2013: 1 · 2012: 4
FWCI
0.85
Type
journal article
Language
en
Open access
Locations
  • Molecular and Cellular Biology (publishedVersion)
  • Europe PMC (PubMed Central) (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
  • Institutional Repositories DataBase (IRDB) (submittedVersion)
Funders
National Institutes of Health
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Microtubule and mitosis dynamics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Cellular transport and secretion
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic and Kidney Cyst Diseases
Keywords
KIF1C, kinesin, molecular motors, Golgi apparatus, retrograde transport, lung fibroblasts, brefeldin A, time-lapse microscopy, organelle distribution
MeSH terms
Amino Acid Sequence, Animals, Base Sequence, Biological Transport, Active, Brain, Cells, Cultured, Cloning, Molecular, Endoplasmic Reticulum, Golgi Apparatus, Molecular Sequence Data, Kinesins, Sequence Homology, Amino Acid, DNA, Complementary, Mice, Knockout, Gene Targeting, Molecular Motor Proteins, Mice

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