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Ciliary kinesins beyond IFT: Cilium length, disassembly, cargo transport and signalling
Author(s) -
Reilly Madeline Louise,
Benmerah Alexandre
Publication year - 2019
Publication title -
biology of the cell
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.543
H-Index - 85
eISSN - 1768-322X
pISSN - 0248-4900
DOI - 10.1111/boc.201800074
Subject(s) - cilium , biology , ciliopathy , ciliopathies , microtubule , microbiology and biotechnology , kinesin , intraflagellar transport , flagellum , ciliogenesis , dynein , basal body , bardet–biedl syndrome , genetics , phenotype , gene
Cilia and flagella are microtubule‐based antenna which are highly conserved among eukaryotes. In vertebrates, primary and motile cilia have evolved to exert several key functions during development and tissue homoeostasis. Ciliary dysfunction in humans causes a highly heterogeneous group of diseases called ciliopathies, a class of genetic multisystemic disorders primarily affecting kidney, skeleton, retina, lung and the central nervous system. Among key ciliary proteins, kinesin family members (KIF) are microtubule‐interacting proteins involved in many diverse cellular functions, including transport of cargo (organelles, proteins and lipids) along microtubules and regulating the dynamics of cytoplasmic and spindle microtubules through their depolymerising activity. Many KIFs are also involved in diverse ciliary functions including assembly/disassembly, motility and signalling. We here review these ciliary kinesins in vertebrates and focus on their involvement in ciliopathy‐related disorders.