Abstract
Recent single-cell studies have revealed that yeast stress response involves transcription factors that are activated in pulses. However, it remains unclear whether and how these dynamic transcription factors temporally interact to regulate stress survival. Here we show that budding yeast cells can exploit the temporal relationship between paralogous general stress regulators, Msn2 and Msn4, during stress response. We find that individual pulses of Msn2 and Msn4 are largely redundant, and cells can enhance the expression of their shared targets by increasing their temporal divergence. Thus, functional redundancy between these two paralogs is modulated in a dynamic manner to confer fitness advantages for yeast cells, which might feed back to promote the preservation of their redundancy. This evolutionary implication is supported by evidence from Msn2/Msn4 orthologs and analyses of other transcription factor paralogs. Together, we show a cell fate control mechanism through temporal redundancy modulation in yeast, which may represent an evolutionarily important strategy for maintaining functional redundancy between gene duplicates.
Highlights
Recent single-cell studies have revealed that yeast stress response involves transcription factors that are activated in pulses
We developed an assay to measure the temporal relationship between Msn2/4 dynamics and the stress survival ability simultaneously at the single-cell level, allowing us to decipher the potential role of temporal redundancy modulation during stress response
In summary, by combining both experiments and mathematical modeling, we have shown that temporal redundancy modulation of the general stress response regulators, Msn[2] and Msn[4], represents a dynamics-based mechanism for cell fate control in budding yeast
Summary
Recent single-cell studies have revealed that yeast stress response involves transcription factors that are activated in pulses. Recent studies have investigated their redundant and divergent roles in target activation[31,35], and an intriguing mechanism based on cisregulatory divergence was proposed to account for the maintenance of functional redundancy between this pair of paralogs[35] It remains largely unclear whether cells could exploit the temporal interactions between these two paralogs to gain fitness advantages, and whether such advantages might be evolutionarily relevant. By integrating single-cell imaging, transcriptome analysis, and mathematical modeling, we show that budding yeast cells can modulate temporal redundancy between Msn[2] and
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