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Mammalian axoneme central pair complex proteins: Broader roles revealed by gene knockout phenotypes
Author(s) -
Teves Maria E.,
NagarkattiGude David R.,
Zhang Zhibing,
Strauss Jerome F.
Publication year - 2016
Publication title -
cytoskeleton
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.95
H-Index - 86
eISSN - 1949-3592
pISSN - 1949-3584
DOI - 10.1002/cm.21271
Subject(s) - axoneme , flagellum , cilium , biology , chlamydomonas , chlamydomonas reinhardtii , microbiology and biotechnology , intraflagellar transport , microtubule , motile cilium , mutant , gene , phenotype , genetics , basal body , model organism
The axoneme genes, their encoded proteins, their functions and the structures they form are largely conserved across species. Much of our knowledge of the function and structure of axoneme proteins in cilia and flagella is derived from studies on model organisms like the green algae, Chlamydomonas reinhardtii . The core structure of cilia and flagella is the axoneme, which in most motile cilia and flagella contains a 9 + 2 configuration of microtubules. The two central microtubules are the scaffold of the central pair complex (CPC). Mutations that disrupt CPC genes in Chlamydomonas and other model organisms result in defects in assembly, stability and function of the axoneme, leading to flagellar motility defects. However, targeted mutations generated in mice in the orthologous CPC genes have revealed significant differences in phenotypes of mutants compared to Chlamydomonas . Here we review observations that support the concept of cell‐type specific roles for the CPC genes in mice, and an expanded repertoire of functions for the products of these genes in cilia, including non‐motile cilia, and other microtubule‐associated cellular functions. © 2016 Wiley Periodicals, Inc.