Kinesin-2 and photoreceptor cell death: Requirement of motor subunits

被引：21

作者：

Jimeno, D

Lillo, C

Roberts, EA

Goldstein, LSB

Williams, DS ^{[1
]}

机构：

[1] Univ Calif San Diego, Dept Pharmacol & Neurosci, Sch Med, La Jolla, CA 92093 USA

[2] Univ Calif San Diego, Sch Med, Howard Hughes Med Inst, Dept Cellular & Mol Med, La Jolla, CA 92093 USA

来源：

EXPERIMENTAL EYE RESEARCH | 2006年 / 82卷 / 02期

关键词：

retina; photoreceptor degeneration; kinesin-2; cilium;

D O I：

10.1016/j.exer.2005.10.026

中图分类号：

R77 [眼科学];

学科分类号：

100212 ;

摘要：

Kinesin-2 function is essential for photoreceptor cell viability. The removal of one of the kinesin-2 motor proteins, KIF3A, by photoreceptorspecific conditional mutagenesis, has been shown to cause rapid photoreceptor cell degeneration. We have explored the possibility that the genes encoding the kinesin-2 motor proteins (KIF3A, K1F3B, and KIF3C) are linked to retinal disease, by examining retinas of knockout mice. We conclude that the reduced KIF3A and KIF3B in heterozygous animals, or the complete absence of KIF3C in homozygous animals does not affect photoreceptor cell survival. Photoreceptor cell death seems to be limited to conditions that, if systemic, are embryonic lethal, indicating that reduced function of the kinesin-2 motor genes is unlikely to underlie inherited retinal degeneration. (c) 2006 Elsevier Ltd. All rights reserved.

引用

页码：351 / 353

页数：3

共 26 条

[1] IFT20 links kinesin II with a mammalian intraflagellar transport complex that is conserved in motile flagella and sensory cilia [J].