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Molecular and Cellular Biology, February 2002, p. 866-873, Vol. 22, No. 3
0270-7306/01/$04.00+0     DOI: 10.1128/MCB.22.3.866-873.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Molecular Motor KIF1C Is Not Essential for Mouse Survival and Motor-Dependent Retrograde Golgi Apparatus-to-Endoplasmic Reticulum Transport

Kazuo Nakajima, Yosuke Takei, Yosuke Tanaka, Terunaga Nakagawa, Takao Nakata, Yasuko Noda, Mitsutoshi Setou, and Nobutaka Hirokawa^*

Department of Cell Biology and Anatomy, Graduate School of Medicine, University of Tokyo, Bunkyo-ku, Tokyo 113-0033, Japan

Received 16 July 2001/ Returned for modification 28 August 2001/ Accepted 30 October 2001

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 KIF1B and to be expressed ubiquitously. To investigate the in vivo significance of KIF1C, we generated kif1C^-/- mice by knocking in the ß-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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* Corresponding author. Mailing address: Department of Cell Biology and Anatomy, Graduate School of Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan. Phone: 81-3-5841-3326. Fax: 81-3-5802-8646. E-mail: hirokawa{at}m.u-tokyo.ac.jp.

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Molecular and Cellular Biology, February 2002, p. 866-873, Vol. 22, No. 3
0022-538X/01/$04.00+0     DOI: 10.1128/MCB.22.3.866-873.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

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