Functional Analysis of Mouse Kinesin Motor Kif3C

Yang, Zhaohuai; Roberts, Elizabeth A.; Goldstein, Lawrence S.B.

doi:10.1128/mcb.21.16.5306-5311.2001

Cited by 51 publications

(36 citation statements)

References 22 publications

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“…The results of our analysis are in agreement with reports that kif3c KO mice are viable and do not display photoreceptor defects (22,23). However, a redundancy of kif3c/kif3b function in photoreceptor cells is surprising in light of previous reports that kif3c is primarily expressed in ganglion cell axons and in amacrine cells (9,10).…”

Section: Discussionsupporting

confidence: 82%

“…The same studies reported that Kif3c is structurally related to Kif3b and, similar to Kif3b, associates with Kif3a, which suggests that Kif3b and Kif3c proteins may function redundantly as alternative binding partners of Kif3a. Although redundancy of kif3b and kif3c function has been hypothesized (9,22), to our knowledge, this is the first study to demonstrate that it actually exists. In the ear, this redundancy is limited to cilia in a subset of auditory hair cells.…”

Section: Discussionmentioning

confidence: 98%

“…The Kif3c kinesin subunit is thought to form complexes with Kif3a (9, 10). Although the mouse Kif3c protein appears to be absent from the photoreceptor cell layer (10,22,23), we considered the possibility that the zebrafish kif3c functions redundantly with kif3b. The zebrafish has two kif3c-related genes, which we will refer to as kif3c and kif3c-like (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…Similar to kif3a, the role of kif3b in different tissues is difficult to evaluate because homozygous mouse mutants die at midgestation, and few, if any, conditional KOs are available (13). The role of kif3c in ciliogenesis also remained obscure, as mouse KOs of this gene do not display any obvious phenotype (22,23). The contribution of kif17 to vertebrate ciliogenesis is even less clear as its studies produced contradictory results (11,24).…”

mentioning

confidence: 99%

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Kinesin-2 family in vertebrate ciliogenesis

Zhao

Omori²,

Brodowska

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

124

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The differentiation of cilia is mediated by kinesin-driven transport. As the function of kinesins in vertebrate ciliogenesis is poorly characterized, we decided to determine the role of kinesin-2 family motors-heterotrimeric kinesin-II and the homodimeric Kif17 kinesin-in zebrafish cilia. We report that kif17 is largely dispensable for ciliogenesis; kif17 homozygous mutant animals are viable and display subtle morphological defects of olfactory cilia only. In contrast to that, the kif3b gene, encoding a heterotrimeric kinesin subunit, is necessary for cilia differentiation in most tissues, although exceptions exist, and include photoreceptors and a subset of hair cells. Cilia of these cell types persist even in kif3b/kif17 double mutants. Although we have not observed a functional redundancy of kif3b and kif17, kif17 is able to substitute for kif3b in some cilia. In contrast to kif3b/kif17 double mutants, simultaneous interference with kif3b and kif3c leads to the complete loss of photoreceptor and hair cell cilia, revealing redundancy of function. This is in agreement with the idea that Kif3b and Kif3c motor subunits form complexes with Kif3a, but not with each other. Interestingly, kif3b mutant photoreceptor cilia differentiate with a delay, suggesting that kif3c, although redundant with kif3b at later stages of differentiation, is not active early in photoreceptor ciliogenesis. Consistent with that, the overexpression of kif3c in kif3b mutants rescues early photoreceptor cilia defects. These data reveal unexpected diversity of functional relationships between vertebrate ciliary kinesins, and show that the repertoire of kinesin motors changes in some cilia during their differentiation. intraflagellar transport | opsin | outer segment | ciliary axoneme

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Section: Discussionsupporting

confidence: 82%

Section: Discussionmentioning

confidence: 98%

Section: Resultsmentioning

confidence: 99%

mentioning

confidence: 99%

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Kinesin-2 family in vertebrate ciliogenesis

Zhao

Omori²,

Brodowska

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

124

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“…The KIF3 KRPs were also detected in testis (24); KIF3A and KIF3B form heterodimers that function as microtubule-based (ϩ)-end transporters of membranous organelles (25). A KIF3C knockout mouse is viable and apparently normal (26). Finally, kinesin II, a member of the KIF3 family, is expressed in developing rat, sea urchin, and sand dollar sperm tails (27,28).…”

mentioning

confidence: 99%

Association of Kinesin Light Chain with Outer Dense Fibers in a Microtubule-independent Fashion

Bhullar

Zhang

Junco

et al. 2003

Journal of Biological Chemistry

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Conventional kinesin I motor molecules are heterotetramers consisting of two kinesin light chains (KLCs) and two kinesin heavy chains. The interaction between the heavy and light chains is mediated by the KLC heptad repeat (HR), a leucine zipper-like motif. Kinesins bind to microtubules and are involved in various cellular functions, including transport and cell division. We recently isolated a novel KLC gene, klc3. klc3 is the only known KLC expressed in post-meiotic male germ cells. A monoclonal anti-KLC3 antibody was developed that, in immunoelectron microscopy, detects KLC3 protein associated with outer dense fibers (ODFs), unique structural components of sperm tails. No significant binding of KLC3 with microtubules was observed with this monoclonal antibody. In vitro experiments showed that KLC3-ODF binding occurred in the absence of kinesin heavy chains or microtubules and required the KLC3 HR. ODF1, a major ODF protein, was identified as the KLC3 binding partner. The ODF1 leucine zipper and the KLC3 HR mediated the interaction. These results identify and characterize a novel interaction between a KLC and a non-microtubule macromolecular structure and suggest that KLC3 could play a microtubule-independent role during formation of sperm tails.

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Kinesin Superfamily Proteins

Hirokawa

Takemura

2008

Protein Science Encyclopedia

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Originally published in: Molecular Motors. Edited by Manfred Schliwa. Copyright © 2003 Wiley‐VCH Verlag GmbH & Co. KGaA Weinheim. Print ISBN: 3‐527‐30594‐0 The sections in this article are Introduction The Kinesin Superfamily Proteins N‐Kinesins N ‐1 Kinesins N ‐2 Kinesins N ‐3 Kinesins The Unc 104/ KIF 1 family The KIF 13 family The KIF 16 family N‐4 Kinesins The KIF 3 family The Osm 3/ KIF 17 family N‐5 Kinesins N‐6 Kinesins The CHO 1/ KIF 23 family The KIF 20/ Rab 6 kinesin family N‐7 Kinesins N‐8 Kinesins The K id/ KIF 22 family The KIF 18 family N ‐9 Kinesins N ‐10 Kinesins N ‐11 Kinesins M‐Kinesins C ‐Kinesins C ‐1 Kinesins C ‐2 Kinesins Orphans Cargoes of KIFs; Specificity and Redundancy Recognition and Binding to Cargoes How to Determine the Direction of Transport

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Functional Analysis of Mouse Kinesin Motor Kif3C

Cited by 51 publications

References 22 publications

Kinesin-2 family in vertebrate ciliogenesis

Kinesin-2 family in vertebrate ciliogenesis

Association of Kinesin Light Chain with Outer Dense Fibers in a Microtubule-independent Fashion

Kinesin Superfamily Proteins

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