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Related Experiment Video

Updated: Mar 17, 2026

Author Spotlight: Evaluation of Protein-Condensate Dynamics in Live Human Cells
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Protein Dimerization Generates Bistability in Positive Feedback Loops.

Chieh Hsu1, Vincent Jaquet2, Mumun Gencoglu2

  • 1Biozentrum, University of Basel, Klingelbergstrasse 50/70, 4056 Basel, Switzerland; School of Biosciences, University of Kent, Canterbury, Kent CT2 7NJ, UK.

Cell Reports
|July 19, 2016
PubMed
Summary
This summary is machine-generated.

Cellular memory relies on bistability, which can be generated by ultrasensitive reactions in transcriptional feedback loops. This study demonstrates how homodimerization and cooperative binding create robust bistability in yeast, independent of cell growth.

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Area of Science:

  • Molecular Biology
  • Systems Biology
  • Genetics

Background:

  • Bistability is crucial for cellular memory and cell-fate decisions.
  • Ultrasensitive molecular reactions within positive feedback loops can generate bistability.
  • Detecting bistability is challenging due to its complex interplay with cellular growth.

Purpose of the Study:

  • To construct and analyze transcriptional feedback loops in yeast to generate and study bistability.
  • To decouple the effects of bistability from cellular growth alterations.
  • To investigate the roles of molecular ultrasensitivity, specifically homodimerization and cooperative binding, in generating robust bistability.

Main Methods:

  • Engineered transcriptional feedback loops in yeast.
  • Tuned translation rates using designed RNA stem loops to control protein levels and eliminate growth effects.
  • Modulated ultrasensitive reactions: transcription factor homodimerization and cooperative promoter binding.

Main Results:

  • Successfully constructed yeast transcriptional feedback loops exhibiting bistability.
  • Demonstrated that either homodimerization or cooperative binding alone is sufficient to induce bistability.
  • Showcased that the combined action of both ultrasensitive mechanisms results in particularly robust bistability.
  • Confirmed that the observed bistability is maintained even when a negative feedback loop is present.

Conclusions:

  • Ultrasensitive molecular reactions, particularly protein homodimerization and cooperative binding, are key drivers of robust cellular bistability.
  • Bistability generated by these mechanisms can be independent of cellular growth effects.
  • The ubiquitous nature of protein homodimerization suggests its significant role in the functional dynamics of biological regulatory networks.