The Journal of Neuroscience, June 7, 2006, ():
Rapid Turnover of Stereocilia Membrane Proteins: Evidence from the Trafficking and Mobility of Plasma Membrane Ca2+-ATPase 2
J. Neurosci. Grati et al.
26: 6386
Supplemental data
Files in this Data Supplement:
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Supplemental figure1
Model of PMCA2 delivery to and removal from the HC stereocilia
Schematic diagram showing the basic organization of the stereocilia bundle and the mechanism for turnover of the stereocilia actin core (modified from Lin et al., 2005) and the turnover of PMCA2 (blue dots). Actin and actin-binding proteins turnover by polymerization at the tip, depolymerization at the base, and continuous treadmilling, which renews the internal structure of the stereocilia. PMCA2 molecules diffuse laterally and are renewed by constant insertion and removal from the apical membrane by the apical trafficking machinery. In this model the PMCA2 molecules randomly move in the apical membrane and in and out of the stereocilia membrane through their narrow tapered base. The lateral diffusion and transient interactions with stereocilia components (orange dots) maintain a high concentration of PMCA2 molecules in the stereocilia and mitigate the futile cycling at the lateral margin of the cell where they are constantly being delivered and removed. EE, early endosome; ER, endoplasmic reticulum.
