My comment: Induced mutations probably mimic what naturally occurs due to nutrient uptake and pheromone-controlled reproduction during seemingly futile thermodynamic cycles of protein biosynthesis and degradation. Cycle frequency that enables short-term epigenetic memory probably links memory in single-celled yeasts to pheromone-controlled adaptive evolution via the cells ability to ‘learn’ which nutrients benefit organism-level thermoregulation sans mutations theory in yeast and every other organism on this planet due to conserved molecular mechanisms. For example see: Stochastic expression and epigenetic memory at the yeast HO promoter PNAS 2013 ; published ahead of print July 8, 2013, doi:10.1073/pnas.1306113110
Abstract: Eukaryotic gene regulation usually involves sequence-specific transcription factors and sequence-nonspecific cofactors. A large effort has been made to understand how these factors affect the average gene expression level among a population. However, little is known about how they regulate gene expression in individual cells. In this work, we address this question by mutating multiple factors in the regulatory pathway of the yeast HO promoter (HOpr) and probing the corresponding promoter activity in single cells using time-lapse fluorescence microscopy. We show that the HOpr fires in an “on/off” fashion in WT cells as well as in different genetic backgrounds. Many chromatin-related cofactors that affect the average level of HO expression do not actually affect the firing amplitude of the HOpr; instead, they affect the firing frequency among individual cell cycles. With certain mutations, the bimodal expression exhibits short-term epigenetic memory across the mitotic boundary. This memory is propagated in “cis” and reflects enhanced activator binding after a previous “on” cycle. We present evidence that the memory results from slow turnover of the histone acetylation marks.
Article excerpt: Most gene expression studies rely on bulk assays to measure the ensemble average of a large quantity of cells. These assays are efficient and insightful, but they tend to mask cell-to-cell variability and asynchronized dynamics among a population. As a result, when a factor is found to affect gene expression, it is generally unknown whether it uniformly affects all cells, changes the fraction of cells that express this gene, or modulates the gene expression dynamics without affecting the actual expression level.
My comment: Masking cell-to-cell variability and asynchronized dynamics among populations of unicellular or multicellular organisms probably led some people to think in terms of mutation-driven evolution, all the while others have recognized for several decades that natural selection for mutations was not possible in accord with the requirements for ecological, social, neurogenic, and socio-cognitive niche construction in adaptive evolution. Besides, changes in cycle frequency enable transmission of epigenetic information about the sensory environment in a manner similar to Morse Code, where pulses can transmit the works of Shakespeare across entire neuronal networks at the same time mutations lead to disease and dead ends. See also: Short-term gene-expression ‘memory’ is inherited in proteins associated with DNA, new research finds
