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Loss of MACF1 Abolishes Ciliogenesis and Disrupts Apicobasal Polarity Establishment in the Retina

Authors :
Helen L. May-Simera
Jessica D. Gumerson
Chun Gao
Maria Campos
Stephanie M. Cologna
Tina Beyer
Karsten Boldt
Koray D. Kaya
Nisha Patel
Friedrich Kretschmer
Matthew W. Kelley
Ronald S. Petralia
Megan G. Davey
Tiansen Li
Source :
Cell Reports, Vol 17, Iss 5, Pp 1399-1413 (2016)
Publication Year :
2016
Publisher :
Elsevier, 2016.

Abstract

Summary: Microtubule actin crosslinking factor 1 (MACF1) plays a role in the coordination of microtubules and actin in multiple cellular processes. Here, we show that MACF1 is also critical for ciliogenesis in multiple cell types. Ablation of Macf1 in the developing retina abolishes ciliogenesis, and basal bodies fail to dock to ciliary vesicles or migrate apically. Photoreceptor polarity is randomized, while inner retinal cells laminate correctly, suggesting that photoreceptor maturation is guided by polarity cues provided by cilia. Deletion of MACF1 in adult photoreceptors causes reversal of basal body docking and loss of outer segments, reflecting a continuous requirement for MACF1 function. MACF1 also interacts with the ciliary proteins MKKS and TALPID3. We propose that a disruption of trafficking across microtubles to actin filaments underlies the ciliogenesis defect in cells lacking MACF1 and that MKKS and TALPID3 are involved in the coordination of microtubule and actin interactions. : May-Simera et al. find that MACF1, a giant protein that mediates microtubule and actin interactions, is essential for ciliogenesis and maintenance. In the developing retina, MACF1 is required for establishing apicobasal polarity in photoreceptors, thus highlighting the importance of cilia in providing the correct positional cues. Keywords: retina, cilia, ciliogenesis, ciliopathy, polarity, retinal degeneration, basal body, centrosome, microtubule, actin

Subjects

Subjects :
Biology (General)
QH301-705.5

Details

Language :
English
ISSN :
22111247
Volume :
17
Issue :
5
Database :
Directory of Open Access Journals
Journal :
Cell Reports
Publication Type :
Academic Journal
Accession number :
edsdoj.37a51d7c3d4235b1f67c2071ed7b25
Document Type :
article
Full Text :
https://doi.org/10.1016/j.celrep.2016.09.089