Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/34786
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Type: Journal article
Title: Regulated cationic channel function in Xenopus oocytes expressing Drosophila big brain
Author: Yanochko, G.
Yool, A.
Citation: Journal of Neuroscience, 2002; 22(7):2530-2540
Publisher: Soc Neuroscience
Issue Date: 2002
ISSN: 0270-6474
1529-2401
Statement of
Responsibility: 
Gina M. Yanochko and Andrea J. Yool
Abstract: Big brain (bib) is a neurogenic gene that when mutated causes defects in cell fate determination during Drosophila neurogenesis through an unknown mechanism. The protein Big Brain (BIB) has sequence identity with the major intrinsic protein family that includes the water- and ion-conducting aquaporin channels. We show here that BIB expressed heterologously in Xenopus oocytes provides a voltage-insensitive, nonselective cation channel function with permeability to K+ > Na+ tetraethylammonium. The conductance, activated in response to endogenous signaling pathways in BIB-expressing oocytes, is decreased after treatment with 20 µM insulin and is enhanced with 10 µM lavendustin A, a tyrosine kinase inhibitor. Western blot analysis confirms that BIB is tyrosine-phosphorylated. Both tyrosine phosphorylation and the potentiating effect of lavendustin A are removed by partial deletion of the C terminus (amino acids 317-700). Current activation is not observed in control oocytes or in oocytes expressing a nonfunctional mutant (BIB E71N) that appears to be expressed on the plasma membrane by confocal microscopy and Western blotting. These results indicate that BIB can participate in tyrosine kinase-regulated transmembrane signaling and may suggest a role for membrane depolarization in the neurogenic function of BIB in early development.
Keywords: major intrinsic protein; Xenopus oocyte; tyrosine kinase; voltage clamp; neurogenic; aquaporin
Description: Copyright © 2002 Society for Neuroscience
RMID: 0020063453
DOI: 10.1523/jneurosci.22-07-02530.2002
Published version: http://www.jneurosci.org/cgi/content/abstract/22/7/2530
Appears in Collections:Molecular and Biomedical Science publications

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