Abstract
BackgroundA prerequisite for a duplication to spread through and persist in a given population is retaining expression of both gene copies. Yet changing a gene's dosage is frequently detrimental to fitness. Consequently, dosage-sensitive genes are less likely to duplicate.However, in cases where the level of gene product is controlled, via negative feedback, by its own abundance, an increase in gene copy number can in principle be decoupled from an increase in protein while both copies remain expressed. Using data from the transcriptional networks of E. coli and S. cerevisiae, we test the hypothesis that genes under negative auto-regulation show enhanced duplicability.ResultsControlling for several known correlates of duplicability, we find no statistically significant support in either E. coli or S. cerevisiae that transcription factors under negative auto-regulation hold a duplicability advantage over transcription factors with no auto-regulation.ConclusionBased on the analysis of transcriptional networks in E. coli and S. cerevisiae, there is no evidence that negative auto-regulation has contributed, on a genome-wide scale, to the variability in gene family sizes in these species.
Highlights
A prerequisite for a duplication to spread through and persist in a given population is retaining expression of both gene copies
Based on the analysis of transcriptional networks in E. coli and S. cerevisiae, there is no evidence that negative auto-regulation has contributed, on a genome-wide scale, to the variability in gene family sizes in these species
No evidence for higher duplicability of negative autoregulators To determine whether genes under homeostatic control exhibit enhanced duplicability, we assessed duplication patterns for genes in the transcription network of E. coli, where a substantial proportion of transcription factors (TFs) (>50%) show negative auto-regulation [12,13]
Summary
A prerequisite for a duplication to spread through and persist in a given population is retaining expression of both gene copies. In cases where the level of gene product is controlled, via negative feedback, by its own abundance, an increase in gene copy number can in principle be decoupled from an increase in protein while both copies remain expressed. As individuals with elevated copy numbers are notably more frequent in populations where these drugs are in use, this suggests the action of natural selection [1]. On a genomewide level, duplicated isozymes in yeast show high retention rates, presumably because increased dosage facilitates high enzymatic flux [2,3]. The authors suggest, decreased fitness is likely owing to overexpression of genes that would normally be expressed only periodically, such as genes involved in the cell cycle [4]. Deleterious effects have been attributed to relative rather than absolute excess in protein, a phenomenon known as dosage imbalance [5,6]
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