Mitochondrial Autophagy

---

Autophagy is an important process for eukaryotes to remove dysfunctional intracellular substances. During the process, some damaged proteins or organelles are wrapped by autophagy vesicles with bilayer membrane structure. Lysosome (in animals) or vacuole (in yeasts and plants) is where the damaged components are degraded and recycled to achieve cell homeostasis and organelle renewal.

The mitochondrion generates chemical energy to power cells' functions and activities, and the energy is stored in the molecule ATP. Mitochondrial damage can lead to the release of ROS or apoptotic factors, resulting in cell injury or apoptosis. Therefore, it is particularly important to remove these damaged mitochondria to maintain the normal function and number of mitochondria, which is usually accomplished by mitochondrial autophagy.

Figure 1. Receptor-mediated mitophagy in yeast and mammalian systems. (Liu L., et al., 2014)

There are pros and cons to mitochondrial autophagy. On the one hand, the normal range of mitochondrial autophagy can maintain the normal physiological function of human cells. On the other hand, too high and low levels of mitochondrial autophagy will cause disease.

Creative Biogene always provides you with customized services for mitochondrial research, and our one-stop research and analysis platform can meet all your research needs.

General Strategy

• MitoTimer

MitoTimer can be used to monitor mitochondrial senescence, renewal, and biogenesis in real-time, and can be used to evaluate the number of individual mitochondria or mitochondria in cells. MitoTimer is a fluorescent reporter protein targeting the mitochondrial matrix.

The MitoTimer is co-located with mitochondria: green mitochondria represent the newly synthesized mitochondria, the red mitochondria represent the old or aging mitochondria, and the yellow mitochondria represent the mature mitochondria.

Because both fluorescence microscopy and flow cytometry can be used for MitoTimer analysis, Creative Biogene uses both methods to monitor the red to green fluorescence of mitochondria, which helps researchers understand the ratio of aging to newly formed mitochondria over time.

• Mt-Keima

Keima targets mitochondria by fusing with mitochondrial matrix to form mt-Keima, Creative Biogene quantifies mitochondria by fluorescence imaging using mitochondrial matrix-targeted mt-Keima fluorescent proteins in vitro and in vivo. Creative Biogene also provides a combination of mt-Keima and GFP-Parkin expression to evaluate mitochondrial activation.

• Mito-QC

Mito-QC consists of a tandem mCherry-GFP tag fused with the mitochondrial targeting sequence of the external mitochondrial membrane protein FIS1. It is a pH-sensitive mitochondrial fluorescence probe.

Mito-QC shows red and green fluorescence under steady-state conditions, but when mitochondrial autophagy is induced, the GFP signal is quenched because the mitochondria are transferred to lysosomes.

Our Advantages

• Rich experience in mitochondrial autophagy detection and analysis
• Outstanding research team
• Unique integrated service for mitochondrial research
• Reliable data and results
• Rapid turnaround and cost-effective

Creative Biogene has the most professional team to serve customers around the world. If you have any questions about the content of this service, please feel free to contact us. We look forward to your contact.

References

1. Sun N., et al. “ Measuring in vivo mitophagy. ” Mol Cell, 2015, 60(4):685-696.
2. Liu L., et al. “ Receptor-mediated mitophagy in yeast and mammalian systems. ” Cell Res, 2014, 24: 787-795.
3. Katayama H., et al. “ A sensitive and quantitative technique for detecting autophagic events based on lysosomal delivery. ” Chem Biol, 2011, 18:1042-1052.
4. McWilliams T.G., et al. “ Mito-QC illuminates mitophagy and mitochondrial architecture in vivo. ” Journal of Cell Biol , 2016, 214: 333-345.
5. Williams J.A., et al. “ New methods for monitoring mitochondrial biogenesis and mitophagy in vitro and in vivo. ” Experimental Biology and Medicine,2017, 242(8): 781-787.

---