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. 2008 Sep 8;182(5):937–950. doi: 10.1083/jcb.200801152

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© 2008 Claypool et al.

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.jcb.org/misc/terms.shtml). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).

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Figure 1. — Disorganization of AAC complexes in the absence of CL. (A) 100 μg of 1.5% (wt/vol) digitonin extracts from mitochondria derived from the indicated strains were resolved by 2D BN/SDS-PAGE and AAC-complexes revealed by immunoblot. n = 3. (B) 25 μg of each subcellular fraction was immunoblotted for the indicated subcellular organelle. n = 2. (C) Steady-state expression was determined from whole cell extracts (5 and 10 μl) by immunoblotting for AAC (bottom), with Taz1p (middle) and Tom70p (top) serving as loading controls. n = 3. (D) CNAPAAC2 assembles in similar complexes as untagged AAC2. n = 3 (E) Serial dilutions of the strains indicated at the left were spotted onto YP medium with dextrose or ethanol–glycerol as the carbon source and incubated at 30°C for 3 d. n = 3. Asterisk highlights cross-reaction with porin of the AAC antiserum.