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. 2017 May 26;68(11):2833–2847. doi: 10.1093/jxb/erx139

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© The Author 2017. Published by Oxford University Press on behalf of the Society for Experimental Biology.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

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Fig. 2. — ORRM5 mutations cause mitochondrial editing defects. Ten sites that experienced a significant decrease of editing extent (Δ ≥10%) upon ORRM5 mutations (left), and ten sites that showed a significant increase of editing extent (Δ ≥10%) in the orrm5 mutants (right). ORRM5-3+/+, wild-type siblings of orrm5-3 mutants; orrm5-3–/–, orrm5-3 homozygous mutants; orrm5-2–/–, orrm5-2 homozygous mutants (n=2). Editing sites are displayed according to the difference between the wild-type and the mutants, from highest to lowest. Values represent mean±SD.