Competition between random genetic drift and natural selection play a central role in evolution: Whereas nonbeneficial mutations often prevail in small populations by chance, mutations that sweep through large populations typically confer a selective advantage. Here, however, we observe chance effects during range expansions that dramatically alter the gene pool even in large microbial populations. Initially well mixed populations of two fluorescently labeled strains of Escherichia coli develop well defined, sector-like regions with fractal boundaries in expanding colonies. The formation of these regions is driven by random fluctuations that originate in a thin band of pioneers at the expanding frontier. A comparison of bacterial and yeast colonies (Saccharomyces cerevisiae) suggests that this large-scale genetic sectoring is a generic phenomenon that may provide a detectable footprint of past range expansions.genetic distance ͉ founder effect ͉ microorganisms ͉ range expansion A principal tenet of modern evolutionary biology is that Darwinian selection and random genetic drift compete in driving evolutionary change (1). It is widely accepted that genetic drift can have significant effects on small populations (2) that may even lead to speciation (3). In large populations, however, random sampling effects are generally considered weak compared with selection (4-6) (law of large numbers). A major departure from this paradigmatic behavior occurs when large populations undergo range expansions. The descendents of individuals first settling in a new territory are most likely to dominate the gene pool as the expansion progresses (7-9). Random sampling effects among these pioneers results in genetic drift that can have profound consequences on the diversity of the expanding population. Indeed, spatially varying levels of genetic diversity and colonization patterns appear to be correlated in many species (10-13). For example, the often observed south-north gradient in neutral genetic diversity [''southern richness to northern purity'' (14)] on the northern hemisphere is thought to reflect past range expansions induced by glacial cycles (12). Although these trends indicate that genetic drift during range expansions has shaped the gene pool of many species, the underlying spatial mechanism remains obscure: Diversity gradients are often difficult to interpret and potentially interfere with the signal of spreading beneficial mutations (15,16). In fact, a major challenge of present-day population genetics is to decide whether natural selection or a past demographic process is responsible for the prevalence of common mutations (17).Here, we use simple microbial systems to study the nature of random genetic drift in range expansions of large populations. We observe chance effects that segregate the gene pool into well defined, sector-like regions of reduced genetic diversity. The genetic segregation on the population level is the consequence of number fluctuations on a much smaller scale, within a thin region of reproducing p...

Summary Cell fate decisions are fundamental for development, but we do not know how cells select between alternate fates. Here, we asked how mouse embryonic stem (ES) cells leave the pluripotent state and choose between germ layer fates. By analyzing the dynamics of the transcriptional circuit that maintains the pluripotent state during lineage choice, we found that the proteins that maintain ES cell identity also orchestrate germ layer fate selection. Core pluripotency factors, Oct4 and Sox2, each suppress differentiation into a single germ layer fate. Differentiation signals continuously and asymmetrically modulate Oct4 and Sox2 protein levels, altering their binding pattern in the genome, and leading to cell fate choice. The same factors that maintain pluripotency, thus, also integrate external signals and control lineage selection. Our study provides a framework for understanding how complex transcription factor networks control cell fate decisions in progenitor cells.