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Gal1 repression memory in budding yeast

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ABSTRACT Cells must continuously adapt to changing environments and, thus, have evolved mechanisms allowing them to respond to repeated stimuli. For example, faster gene induction upon a repeated stimulus aids adaptation - a process known as reinduction memory. However, whether such a memory exists for gene repression is unclear. Here, we studied gene repression across repeated carbon source shifts in over 2,500 single Saccharomyces cerevisiae cells. By monitoring the expression of a carbon source-responsive gene, galactokinase 1 ( Gal1 ), and mathematical modeling, we discovered repression memory at the population and single-cell level. Using a repressor model to estimate single-cell repression parameters, we show that repression memory is due to a shortened repression delay, the estimated time gap between carbon source shift and Gal1 expression termination, upon the repeated carbon source shift. Additionally, we show that cells lacking Elp6 display a gain-of-repression-memory phenotype characterized by a stronger decrease in repression delay between two consecutive carbon source shifts. Collectively, our study provides the first quantitative description of repression memory in single cells.
Title: Gal1 repression memory in budding yeast
Description:
ABSTRACT Cells must continuously adapt to changing environments and, thus, have evolved mechanisms allowing them to respond to repeated stimuli.
For example, faster gene induction upon a repeated stimulus aids adaptation - a process known as reinduction memory.
However, whether such a memory exists for gene repression is unclear.
Here, we studied gene repression across repeated carbon source shifts in over 2,500 single Saccharomyces cerevisiae cells.
By monitoring the expression of a carbon source-responsive gene, galactokinase 1 ( Gal1 ), and mathematical modeling, we discovered repression memory at the population and single-cell level.
Using a repressor model to estimate single-cell repression parameters, we show that repression memory is due to a shortened repression delay, the estimated time gap between carbon source shift and Gal1 expression termination, upon the repeated carbon source shift.
Additionally, we show that cells lacking Elp6 display a gain-of-repression-memory phenotype characterized by a stronger decrease in repression delay between two consecutive carbon source shifts.
Collectively, our study provides the first quantitative description of repression memory in single cells.

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