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. 2008 Sep 29;205(10):2397–2408. doi: 10.1084/jem.20081297

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© 2008 Chen 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.jem.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 6. — Up-regulated mitochondrial biogenesis in Tsc1-deficient, FLSKCD48⁻ HSCs. (a) Tsc1 deletion results in increased mitochondrial biogenesis, as revealed by increased MitoTracker Green–high populations. (left) A representative FACS profile from one mouse BM LT-HSC is shown (numbers indicate percentages). (right) The summary data (means ± SD; n = 4) of the percentage of cells with high mitochondrion contents are shown. (b) Relative mitochondrion DNA contents in WT and Tsc1-deficient LT-HSCs. Mitochondrial DNA and genomic DNA were extracted from HSCs, and the copy number of mitochondrial DNA was measured by RT-PCR, normalized to genomic DNA. As a Ctrl, the mitochondrial DNA copy numbers from the tails of the Ctrl and mutant mice are measured. The mean abundance in Ctrl HSCs was defined as 1. Data shown are means ± SD (n = 3). (c) Up-regulation of the expressions of mitochondrial genes involved in oxidative phosphorylation in Tsc1-deficient HSCs. The mRNA levels of mitochondrial genes (Cyt C, Cox5a, UCP3, Hdufs8, Idh3a, and Atp5g1) are measured by real-time RT-PCR. Data shown were means ± SD of the fraction of Hprt copy numbers (n = 4). The data presented in this figure have been reproduced in at least four experiments.