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Published on: September 6, 2024
Target of Rapamycin Complex 2 regulates cell growth via Myc in Drosophila
Ying Kuo1, Huanwei Huang1, Tao Cai1
1National Institute of Biological Sciences, Beijing, China.
Abstract:
Target of rapamycin (TOR) is an evolutionarily conserved serine/threonine protein kinase that functions as a central regulator of cellular growth and metabolism by forming two distinct complexes: TOR complex 1 (TORC1) and TORC2. As well as TORC1, TORC2 plays a key role in regulation of cell growth. But little is known about how TORC2 regulates cell growth. The transcription factor Myc also plays a critical role in cell proliferation and growth. Here we report that TORC2 and Myc regulate cell growth via a common pathway. Expression of Myc fully rescued growth defects associated with lst8 and rictor mutations, both of which encode essential components of TORC2. Furthermore, loss of TORC2 disrupted the nuclear localization of Myc, and inhibited Myc-dependent transcription. Together, our results reveal a Myc-dependent pathway by which TORC2 regulates cell growth.
Insights
Target of rapamycin complex 2 (TORC2) and the transcription factor Myc share a common pathway to regulate cell growth. TORC2 influences Myc
Area of Science:
- Cellular Biology
- Molecular Biology
- Biochemistry
Background:
- Target of rapamycin (TOR) is a conserved kinase regulating cell growth and metabolism.
- TOR forms two complexes, TORC1 and TORC2, with distinct functions.
- TORC2's role in cell growth regulation is not fully understood, unlike TORC1.
- The transcription factor Myc is crucial for cell proliferation and growth.
Purpose of the Study:
- To investigate the relationship between TORC2 and Myc in cell growth regulation.
- To elucidate the molecular mechanisms by which TORC2 controls cell growth.
Main Methods:
- Genetic analysis of TORC2 components (lst8, rictor) and Myc.
- Assessment of cell growth defects and rescue experiments.
- Analysis of Myc's nuclear localization and transcriptional activity.
Main Results:
- Myc expression rescued growth defects caused by mutations in TORC2 components.
- Loss of TORC2 impaired Myc's nuclear localization.
- TORC2 deficiency inhibited Myc-dependent gene transcription.
- A novel Myc-dependent pathway for TORC2-mediated cell growth was identified.
Conclusions:
- TORC2 and Myc collaborate in a common pathway to regulate cell growth.
- TORC2 impacts cell growth by modulating Myc's activity and localization.
- This study reveals a new mechanism for TORC2 in controlling cellular processes.
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