Partially Redundant Actin Genes in Chlamydomonas Control Transition Zone Organization and Flagellum-Directed Traffic.
| Autor: | Jack B; Department of Anatomy and Cell Biology, University of Kansas Medical Center, Kansas City, KS 66160, USA., Mueller DM; Department of Anatomy and Cell Biology, University of Kansas Medical Center, Kansas City, KS 66160, USA., Fee AC; University of Missouri-Kansas City, School of Medicine, Kansas City, MO 64110, USA., Tetlow AL; Department of Anatomy and Cell Biology, University of Kansas Medical Center, Kansas City, KS 66160, USA., Avasthi P; Department of Anatomy and Cell Biology, University of Kansas Medical Center, Kansas City, KS 66160, USA; Department of Ophthalmology, University of Kansas Medical Center, Kansas City, KS 66160, USA. Electronic address: pavasthi@kumc.edu. |
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| Jazyk: | angličtina |
| Zdroj: | Cell reports [Cell Rep] 2019 May 21; Vol. 27 (8), pp. 2459-2467.e3. |
| DOI: | 10.1016/j.celrep.2019.04.087 |
| Abstrakt: | The unicellular green alga Chlamydomonas reinhardtii is a biflagellated cell with two actin genes: one encoding a conventional actin (IDA5) and the other encoding a divergent novel actin-like protein (NAP1). Here, we probe how actin redundancy contributes to flagellar assembly. Disrupting a single actin allows complete flagellar assembly. However, when disrupting both actins using latrunculin B (LatB) treatment on the nap1 mutant background, we find that actins are necessary for flagellar growth from newly synthesized limiting flagellar proteins. Under total actin disruption, transmission electron microscopy identified an accumulation of Golgi-adjacent vesicles. We also find that there is a mislocalization of a key transition zone gating and ciliopathy protein, NPHP-4. Our experiments demonstrate that each stage of flagellar biogenesis requires redundant actin function to varying degrees, with an absolute requirement for these actins in transport of Golgi-adjacent vesicles and flagellar incorporation of newly synthesized proteins. (Copyright © 2019 The Author(s). Published by Elsevier Inc. All rights reserved.) |
| Databáze: | MEDLINE |
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