| Project/Area Number |
21K20632
|
|---|
| Research Category |
Grant-in-Aid for Research Activity Start-up
|
| Allocation Type | Multi-year Fund |
|---|
| Review Section |
0701:Biology at molecular to cellular levels, and related fields
|
|---|
| Research Institution | Niigata University |
|---|
Principal Investigator |
|
|---|
| Project Period (FY) |
2021-08-30 – 2023-03-31
|
| Project Status |
Completed (Fiscal Year 2022)
|
| Budget Amount *help |
¥3,120,000 (Direct Cost: ¥2,400,000、Indirect Cost: ¥720,000)
Fiscal Year 2022: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2021: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
|
|---|
| Keywords | Mitophagy / Atg32 / Ppg1 / The Far complex / Yeast / Autophagy |
|---|
| Outline of Research at the Start |
Mitophagy contributes to maintaining mitochondrial quality and quantity. The phosphorylation of the mitophagy receptor Atg32 is essential for mitophagy and antagonistically regulated by CK2 and Ppg1. The Ppg1-binding partner Far complex interacts with Atg32 and this interaction is impaired upon mitophagy stimuli, leading to Atg32 phosphorylation, but the underlying mechanism still unclear. To investigate the Far complex-mediated mitophagy regulation in yeast, this study aims to elucidate: ① How the Far complex and Atg32 interact; ② the upstream signalling pathway regulating this interaction.
|
| Outline of Final Research Achievements |
Mitophagy is crucial for maintaining mitochondrial quality and quantity, with phosphorylation of Atg32 being an essential step. However, the underlying mechanism of the Far complex's interaction with Atg32 to phosphorylate it is still unclear. This study aimed to elucidate the interaction between the Far complex and Atg32, as well as the upstream signaling pathway regulating it. The study found that substitution mutants of Far8 phosphorylation sites do not affect Atg32 phosphorylation status or Far8-Atg32 interaction. Additionally, the study discovered that Far3 and Far7 are necessary for Far8-Atg32 interaction. The study also checked the influence of the expression level or degradation of Far8, as well as the influence of a set of kinases involved in autophagy, but neither seemed to affect the Atg32-Far8 interaction.
|
| Academic Significance and Societal Importance of the Research Achievements |
This research could help researchers understand regulation of autophagy, mitophagy in particular. These findings could also lead to new insights into cellular signaling pathways and potentially aid in the development of new therapeutics for diseases caused by mitochondrial dysfunction.
|
