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. 2013 Feb;12(2):343–355. doi: 10.1128/EC.00304-12

Fig 5.

Fig 5

TbERV1 depletion causes mitochondrial swelling. (A) The thin-section electron micrograph of a longitudinal section through a parental T. brucei procyclic cell shows the normal morphology of the mitochondrion. (B) A thin-section micrograph reveals discernible mitochondrial swelling of a procyclic TbERV1 RNAi mutant in the noninduced state. (C) Intact kinetoplast DNA disk in a noninduced procyclic TbERV1 RNAi mutant. (D) Massive mitochondrial swelling in TbERV1 procyclic RNAi mutants 72 h after the induction of RNAi. (E) Intact kinetoplast DNA disk in a procyclic TbERV1 RNAi mutant 72 h after RNAi induction. (F) Longitudinal section revealing normal mitochondrial morphology in a bloodstream-form trypomastigote cell. (G) Thin-section micrograph showing normal mitochondrial morphology of a bloodstream-form TbERV1 RNAi mutant in the noninduced state. (H) Conspicuous mitochondrial swelling in a TbERV1 bloodstream-form RNAi mutant 72 h post-RNAi induction. Scale bars represent 1 μm (A, B, D, F, G, and H) and 200 nm (C and E). Arrows point to the kinetoplast; open triangles designate the mitochondrion.