期刊
JOURNAL OF CELL BIOLOGY
卷 214, 期 3, 页码 333-345出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1083/jcb.201603039
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资金
- AstraZeneca
- Boehringer-Ingelheim
- GlaxoSmithKline
- Merck KGaA
- Janssen Pharmaceutica
- Pfizer
- Medical Research Council [MC_UU_12016/4]
- Wellcome Trust [101022/Z/13/Z]
- Medical Research Council [1646339, MC_UU_12016/4] Funding Source: researchfish
- Parkinson's UK [G-1506, H-1403] Funding Source: researchfish
- MRC [MC_UU_12016/4] Funding Source: UKRI
- Wellcome Trust [101022/Z/13/Z] Funding Source: Wellcome Trust
Autophagic turnover of mitochondria, termed mitophagy, is proposed to be an essential quality-control (QC) mechanism of pathophysiological relevance in mammals. However, if and how mitophagy proceeds within specific cellular subtypes in vivo remains unclear, largely because of a lack of tractable tools and models. To address this, we have developed mito-QC, a transgenic mouse with a pH-sensitive fluorescent mitochondrial signal. This allows the assessment of mitophagy and mitochondrial architecture in vivo. Using confocal microscopy, we demonstrate that mito-QC is compatible with classical and contemporary techniques in histochemistry and allows unambiguous in vivo detection of mitophagy and mitochondrial morphology at single-cell resolution within multiple organ systems. Strikingly, our model uncovers highly enriched and differential zones of mitophagy in the developing heart and within specific cells of the adult kidney. mito-QC is an experimentally advantageous tool of broad relevance to cell biology researchers within both discovery-based and translational research communities.
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