<i>mito</i>-QC illuminates mitophagy and mitochondrial architecture in vivo

McWilliams, Thomas G.; Prescott, Alan R.; Allen, Geoffrey; Tamjar, J.; Munson, Michael J.; Thomson, Calum; Muqit, Miratul M. K.; Ganley, Ian G.

doi:10.1083/jcb.201603039

Cited by 395 publications

(440 citation statements)

References 44 publications

Supporting

Mentioning

397

Contrasting

Order By: Relevance

“…McWilliams et al determined that mitophagy occurs at similar rates in heart and skeletal muscle using mito-QC mice. 37 They also showed that lowest levels of mitophagy occurred in the spleen while highest levels of mitophagy occurred in the liver and kidney among the tissues analyzed. Interestingly, high expression levels of mitophagy were also seen in the muscle fibers of the tongue in mito-QC mice.…”

Section: Mito-qcmentioning

confidence: 99%

“…Interestingly, high expression levels of mitophagy were also seen in the muscle fibers of the tongue in mito-QC mice. 37 An advantage of mito-QC is that mitochondria populations within different areas of a particular tissue can be monitored. For example, young mice had higher mitophagy levels in their kidney glomeruli while adult mice had lower levels of mitophagy in their glomeruli and higher levels in their cortical tubules.…”

Section: Mito-qcmentioning

confidence: 99%

“…Entire mitochondrial networks can also be compared using mito-QC mice. 37 In addition, mito-QC mice can be used to monitor changes in mitophagy during stress. Treatment of MEFs isolated from mito-QC mice with the iron chelator deferiprone significantly increased the levels of mCherry puncta compared to control cells, indicative of increased mitophagy levels.…”

Section: Mito-qcmentioning

confidence: 99%

“…Mito-QC does not seem to affect mitochondrial structure or function. 37 Mito-QC mice have been used for monitoring mitophagy levels during stress in addition to comparing mitochondrial networks and mitophagy levels among different tissues. McWilliams et al determined that mitophagy occurs at similar rates in heart and skeletal muscle using mito-QC mice.…”

Section: Mito-qcmentioning

confidence: 99%

“…Therefore, mCherry-only puncta are seen during mitophagy activation. 37 Mito-QC transgenic mice were developed by knockin of mCherry-GFP-FIS1101-152 in the Rosa26 locus of C57BL/6 mice, which allows expression of mito-QC in all mammalian tissues. However, expression levels of the transgene vary between heart, skeletal muscle, and liver with lowest expression in the liver.…”

Section: Mito-qcmentioning

confidence: 99%

See 4 more Smart Citations

New methods for monitoring mitochondrial biogenesis and mitophagy in vitro and in vivo

Williams

Zhao

Jin

et al. 2017

Exp Biol Med (Maywood)

View full text Add to dashboard Cite

Removal of damaged mitochondria through mitophagy is critical for maintaining cellular homeostasis and functions. However, reliable quantitative assays to monitor mitophagy, particularly in vivo, are just emerging. This review will summarize the current novel quantitative assays to monitor mitophagy in vivo. AbstractRemoval of damaged mitochondria through mitophagy is critical for maintaining cellular homeostasis and functions. Increasing evidence implicates mitophagy in red blood cell differentiation, neurodegeneration, macrophage-mediated inflammation, ischemia, adipogenesis, drug-induced tissue injury, and cancer. Considerable progress has been made toward understanding the biochemical mechanisms involved in mitophagy regulation. However, few reliable assays to monitor and quantify mitophagy have been developed, particularly in vivo. In this review, we summarize the recent development of three assays, MitoTimer, mt-Keima and mito-QC, for monitoring and quantifying mitophagy in cells and in animal tissues. We also discuss the advantages and limitations of these three assays when using them to monitor and quantify mitophagy.

show abstract

Section: Mito-qcmentioning

confidence: 99%

Section: Mito-qcmentioning

confidence: 99%

Section: Mito-qcmentioning

confidence: 99%

Section: Mito-qcmentioning

confidence: 99%

Section: Mito-qcmentioning

confidence: 99%

See 3 more Smart Citations

New methods for monitoring mitochondrial biogenesis and mitophagy in vitro and in vivo

Williams

Zhao

Jin

et al. 2017

Exp Biol Med (Maywood)

View full text Add to dashboard Cite

show abstract

Mitochondrial clearance: mechanisms and roles in cellular fitness

Onishi

Okamoto

2021

FEBS Letters

View full text Add to dashboard Cite

Edited by Agnieszka ChacinskaMitophagy is one of the selective autophagy pathways that catabolizes dysfunctional or superfluous mitochondria. Under mitophagy-inducing conditions, mitochondria are labeled with specific molecular landmarks that recruit the autophagy machinery to the surface of mitochondria, enclosed into autophagosomes, and delivered to lysosomes (vacuoles in yeast) for degradation. As damaged mitochondria are the major sources of reactive oxygen species, mitophagy is critical for mitochondrial quality control and cellular health. Moreover, appropriate control of mitochondrial quantity via mitophagy is vital for the energy supply-demand balance in cells and whole organisms, cell differentiation, and developmental programs. Thus, it seems conceivable that defects in mitophagy could elicit pleiotropic pathologies such as excess inflammation, tissue injury, neurodegeneration, and aging. In this review, we will focus on the molecular basis and physiological relevance of mitophagy, and potential of mitophagy as a therapeutic target to overcome such disorders.

show abstract

Autophagy at the intersection of aging, senescence, and cancer

Cassidy

Narita

2022

Molecular Oncology

View full text Add to dashboard Cite

Autophagy is an evolutionarily conserved cellular process in which macromolecules undergo lysosomal degradation. It fulfills essential roles in quality controlling cellular constituents and in energy homeostasis. Basal autophagy is also widely accepted to provide a protective role in aging and aging-related disorders, and its decline with age might precipitate the onset of a variety of diseases. In this review, we discuss the role of basal autophagy in maintaining homeostasis, in part through the maintenance of stem cell populations and the prevention of cellular senescence. We also consider how stress-induced senescence, for example, during oncogene activation and in premalignant disease, might rely on autophagy, and the possibility that the age-associated decline in autophagy might promote tumour development through a variety of mechanisms. Ultimately, evidence suggests that autophagy is required for malignant cancer progression in a number of settings. Thus, autophagy appears to be tumour-suppressive during the early stages of tumorigenesis and tumour-promoting at later stages.

show abstract

mito-QC illuminates mitophagy and mitochondrial architecture in vivo

Cited by 395 publications

References 44 publications

New methods for monitoring mitochondrial biogenesis and mitophagy in vitro and in vivo

New methods for monitoring mitochondrial biogenesis and mitophagy in vitro and in vivo

Mitochondrial clearance: mechanisms and roles in cellular fitness

Autophagy at the intersection of aging, senescence, and cancer

Contact Info

Product

Resources

About