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Published on: October 17, 2019
Max-independent functions of Myc in Drosophila melanogaster
Dominik Steiger1, Michael Furrer, Daniela Schwinkendorf
1Zoologisches Institut, Universitat Zurich, Winterthurerstrasse 190, 8057 Zurich, Switzerland.
Abstract:
Myc proteins are powerful proto-oncoproteins and important promoters of growth and proliferation during normal development. They are thought to exercise their effects upon binding to their partner protein Max, and their activities are largely antagonized by complexes of Max with Mnt or an Mxd family protein. Although the biological functions of Myc, Mxd and Mnt have been intensively studied, comparatively little is known about the in vivo role of Max. Here we generate Max loss-of-function and reduction-of-function mutations in Drosophila melanogaster to address the contribution of Max to Myc-dependent growth control. We find that many biological activities of Myc do not, or only partly, require the association with Max--for example, the control of endoreplication and cell competition-and that a Myc mutant that does not interact with Max retains substantial biological activity. We further show that Myc can control RNA polymerase III independently of Max, which explains some of Myc's observed biological activities. These studies show the ability of Myc to function independently of Max in vivo and thus change the current model of Max network function.
Insights
The study reveals that Myc proteins can drive cell growth independently of their partner protein Max. This finding challenges the established model of Myc-Max network function in vivo.
Area of Science:
- Molecular Biology
- Genetics
- Developmental Biology
Background:
- Myc proteins are proto-oncoproteins crucial for cell growth and proliferation.
- Myc typically functions by binding to the partner protein Max.
- The in vivo role of Max in Myc's biological activities remains largely uncharacterized.
Purpose of the Study:
- To investigate the in vivo role of Max in Myc-dependent growth control.
- To determine the extent to which Myc requires Max association for its functions.
- To elucidate the current model of Max network function.
Main Methods:
- Generation of Max loss-of-function and reduction-of-function mutations in Drosophila melanogaster.
- Analysis of Myc's biological activities, including endoreplication and cell competition.
- Assessment of Myc's ability to control RNA polymerase III.
Main Results:
- Many Myc activities, such as controlling endoreplication and cell competition, do not require Max association.
- A Myc mutant unable to interact with Max retains significant biological activity.
- Myc demonstrates the capacity to regulate RNA polymerase III independently of Max.
Conclusions:
- Myc can function independently of Max in vivo, challenging the current understanding of the Myc-Max network.
- The findings suggest Myc possesses Max-independent mechanisms for controlling cellular processes.
- This study redefines the functional network of Max in regulating Myc's biological roles.
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