Chlamydomonas PKD2 organizes mastigonemes, hair-like glycoprotein polymers on cilia

Mutations in the channel protein PKD2 cause autosomal dominant polycystic kidney disease, but the function of PKD2 in cilia remains unclear. Here, we show that PKD2 targets and anchors mastigonemes, filamentous polymers of the glycoprotein MST1, to the extracellular surface of Chlamydomonas cilia. P...

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Bibliographic Details
Published in:The Journal of cell biology 2020-06, Vol.219 (6), p.1
Main Authors: Liu, Peiwei, Lou, Xiaochu, Wingfield, Jenna L, Lin, Jianfeng, Nicastro, Daniela, Lechtreck, Karl
Format: Article
Language:English
Subjects:
Axoneme - metabolism
Cell Movement - genetics
Cell Movement - physiology
Chlamydomonas
Chlamydomonas - genetics
Chlamydomonas - metabolism
Chlamydomonas - physiology
Cilia
Cilia - metabolism
Glycoproteins
Glycoproteins - metabolism
Kidney diseases
Mutants
Mutation
Polycystic kidney
Polymers
Polymers - metabolism
Structural Biology
Supports
Transient Receptor Potential Channels - genetics
Transient Receptor Potential Channels - metabolism
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Summary:Mutations in the channel protein PKD2 cause autosomal dominant polycystic kidney disease, but the function of PKD2 in cilia remains unclear. Here, we show that PKD2 targets and anchors mastigonemes, filamentous polymers of the glycoprotein MST1, to the extracellular surface of Chlamydomonas cilia. PKD2-mastigoneme complexes physically connect to the axonemal doublets 4 and 8, positioning them perpendicular to the plane of ciliary beating. pkd2 mutant cilia lack mastigonemes, and mutant cells swim with reduced velocity, indicating a motility-related function of the PKD2-mastigoneme complex. Association with both the axoneme and extracellular structures supports a mechanosensory role of Chlamydomonas PKD2. We propose that PKD2-mastigoneme arrays, on opposing sides of the cilium, could perceive forces during ciliary beating and transfer these signals to locally regulate the response of the axoneme.
ISSN:0021-9525
1540-8140
DOI:10.1083/jcb.202001122