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Hallatschek, O.

Publications and source records attributed to Hallatschek, O..

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Spatial soft sweeps: patterns of adaptation in populations with long-range dispersal

Adaptation in extended populations often occurs through multiple independent mutations responding in parallel to a common selection pressure. As the mutations spread concurrently through the population, they leave behind characteristic patterns of polymorphism near selected loci--so-called soft sweeps--which remain visible after adaptation is complete. These patterns are well-understood in two limits of the spreading dynamics of beneficial mutations: the panmictic case with complete absence of spatial structure, and spreading via short-ranged or diffusive dispersal events, which tessellates space into distinct compact regions each descended from a unique mutation. However, spreading behaviour in most natural populations is not exclusively panmictic or diffusive, but incorporates both short-range and long-range dispersal events. Here, we characterize the spatial patterns of soft sweeps driven by dispersal events whose jump distances are broadly distributed, using lattice-based simulations and scaling arguments. We find that mutant clones adopt a distinctive structure consisting of compact cores surrounded by fragmented \"haloes\" which mingle with haloes from other clones. As long-range dispersal becomes more prominent, the progression from diffusive to panmictic behaviour is marked by two transitions separating regimes with differing relative sizes of halo to core. We analyze the implications of the core-halo structure for the statistics of soft sweep detection in small genomic samples from the population, and find opposing effects of long-range dispersal on the expected diversity in global samples compared to local samples from geographic subregions of the range. We also discuss consequences of the standing genetic variation induced by the soft sweep on future adaptation and mixing.

evolutionary biology

Directional selection limits ecological diversification and promotes ecological tinkering during the competition for substitutable resources

Microbial communities can evade competitive exclusion by diversifying into distinct ecological niches. This spontaneous diversification often occurs amid a backdrop of directional selection on other microbial traits, where competitive exclusion would normally apply. Yet despite their empirical relevance, little is known about how diversification and directional selection combine to determine the ecological and evolutionary dynamics within a community. To address this gap, we introduce a simple, empirically motivated model of eco-evolutionary feedback based on the competition for substitutable resources. Individuals acquire heritable mutations that alter resource uptake rates, either by shifting metabolic effort between resources or by increasing overall fitness. While these constitutively beneficial mutations are trivially favored to invade, we show that the accumulated fitness differences can dramatically influence the ecological structure and evolutionary dynamics that emerge within the community. Competition between ecological diversification and ongoing fitness evolution leads to a state of diversification-selection balance, in which the number of extant ecotypes can be pinned below the maximum capacity of the ecosystem, while the ecotype frequencies and genealogies are constantly in flux. Interestingly, we find that fitness differences generate emergent selection pressures to shift metabolic effort toward resources with lower effective competition, even in saturated ecosystems. We argue that similar dynamical features should emerge in a wide range of models with a mixture of directional and diversifying selection.

evolutionary biology

Collective motion conceals fitness differences in crowded cellular populations

Many cellular populations are tightly-packed, for example microbial colonies and biofilms [39, 10, 41], or tissues and tumors in multi-cellular organisms [11, 29]. Movement of one cell inside such crowded assemblages requires movement of others, so that cell displacements are correlated over many cell diameters [28, 6, 31]. Whenever movement is important for survival or growth [15, 34, 38, 9], such correlated rearrangements could couple the evolutionary fate of different lineages. Yet, little is known about the interplay between mechanical stresses and evolution in dense cellular populations. Here, by tracking deleterious mutations at the expanding edge of yeast colonies, we show that crowding-induced collective motion prevents costly mutations from being weeded out rapidly. Joint pushing by neighboring cells generates correlated movements that suppress the differential displacements required for selection to act. Such mechanical screening of fitness differences allows the mutants to leave more descendants than expected under non-mechanical models, thereby increasing their chance for evolutionary rescue [2, 5]. Our work suggests that mechanical interactions generally influence evolutionary outcomes in crowded cellular populations, which has to be considered when modeling drug resistance or cancer evolution [1, 22, 34, 30, 36, 42].

biophysics

Evolutionary dynamics of bacteria in the gut microbiome within and across hosts

Gut microbiota are shaped by a combination of ecological and evolutionary forces. While the ecological dynamics have been extensively studied, much less is known about how species of gut bacteria evolve over time. Here we introduce a model-based framework for quantifying evolutionary dynamics within and across hosts using a panel of metagenomic samples. We use this approach to study evolution in [~]30 prevalent species in the human gut. Although the patterns of between-host diversity are consistent with quasi-sexual evolution and purifying selection on long timescales, we identify new genealogical signatures that challenge standard population genetic models of these processes. Within hosts, we find that genetic differences that accumulate over [~]6 month timescales are only rarely attributable to replacement by distantly related strains. Instead, the resident strains more commonly acquire a smaller number of putative evolutionary changes, in which nucleotide variants or gene gains or losses rapidly sweep to high frequency. By comparing these mutations with the typical between-host differences, we find evidence that some sweeps are seeded by recombination, in addition to new mutations. However, comparisons of adult twins suggest that replacement eventually overwhelms evolution over multi-decade timescales, hinting at fundamental limits to the extent of local adaptation. Together, our results suggest that gut bacteria can evolve on human-relevant timescales, and they highlight the connections between these short-term evolutionary dynamics and longer-term evolution across hosts.

evolutionary biology

Neither pulled nor pushed: Genetic drift and front wandering uncover a new class of reaction-diffusion waves

Short AbstractTraveling waves describe diverse natural phenomena from crystal growth in physics to range expansions in biology. Two classes of waves exist with very different properties: pulled and pushed. Pulled waves are driven by high growth rates at the expansion edge, where the number of organisms is small and fluctuations are large. In contrast, fluctuations are suppressed in pushed waves because the region of maximal growth is shifted towards the population bulk. Although it is commonly believed that expansions are either pulled or pushed, we found an intermediate class of waves with bulk-driven growth, but exceedingly large fluctuations. These waves are unusual because their properties are controlled by both the leading edge and the bulk of the front.\n\nLong AbstractEpidemics, flame propagation, and cardiac rhythms are classic examples of reaction-diffusion waves that describe a switch from one alternative state to another. Only two types of waves are known: pulled, driven by the leading edge, and pushed, driven by the bulk of the wave. Here, we report a distinct class of semi-pushed waves for which both the bulk and the leading edge contribute to the dynamics. These hybrid waves have the kinetics of pushed waves, but exhibit giant fluctuations similar to pulled waves. The transitions between pulled, semi-pushed, and fully-pushed waves occur at universal ratios of the wave velocity to the Fisher velocity. We derive these results in the context of a species invading a new habitat by examining front diffusion, rate of diversity loss, and fluctuation-induced corrections to the expansion velocity. All three quantities decrease as a power law of the population density with the same exponent. We analytically calculate this exponent taking into account the fluctuations in the shape of the wave front. For fully-pushed waves, the exponent is -1 consistent with the central limit theorem. In semi-pushed waves, however, the fluctuations average out much more slowly, and the exponent approaches 0 towards the transition to pulled waves. As a result, a rapid loss of genetic diversity and large fluctuations in the position of the front occur even for populations with cooperative growth and other forms of an Allee effect. The evolutionary outcome of spatial spreading in such populations could therefore be less predictable than previously thought.

ecology

Selection-like biases emerge in population models with recurrent jackpot events

Evolutionary dynamics driven out of equilibrium by growth, expansion or adaptation often generate a characteristically skewed distribution of descendant numbers: The earliest, the most advanced or the fittest ancestors have exceptionally large number of descendants, which Luria and Delbruck called \"jackpot\" events. Here, we show that recurrent jackpot events generate a deterministic bias favoring majority alleles, which is equivalent to an effective frequency-dependent selection (proportional to the log ratio of the frequencies of mutant and wild-type alleles). This \"fictitious\" selection force results from the fact that majority alleles tend to sample deeper into the tail of the descendant distribution. The flipside of this sampling effect is the rare occurrence of large frequency hikes in favor of minority alleles, which ensures that the allele frequency dynamics remains neutral overall unless genuine selection is present. The limiting allele frequency process is dual to the Bolthausen-Sznitman coalescent and has a particularly simple representation in terms of the logarithm of the mutant frequency. The resulting picture of a selection-like bias compensated by rare big jumps allows for an intuitive understanding of allele frequency trajectories and enables the exact calculation of transition densities for a range of important scenarios, including population size changes and different forms of selection. The fixation of unconditionally beneficial mutations is shown to be exponentially suppressed and balancing selection can maintain diversity only if the population size is large enough. We briefly discuss analogous effects in disordered complex systems, where sampling-induced biases can be viewed as ergodicity breaking driving forces.\n\nOne of the virtues of mathematizing Darwins theory of evolution is that one obtains quantitative predictions about the dynamics of allele frequencies that can be tested with increasing rigor as experimental techniques, sequencing methods and computational power advance. The Wright-Fisher model is arguably the simplest null model of how allele frequencies change across time [17]. Although, for modeling neutral genetic diversity, it is often replaced by equivalent backward-in-time models of the ensuing tree structures [23], forward-in-time approaches are still unrivaled in their ability to include the effects of natural selection. As such, the Wright-Fisher model has been instrumental for shaping the intuition of generations of population genetics about the basic dynamics of neutral and selected variants. But transition densities derived from the Wright-Fisher model also find tangible application in scans for selection in time series data [4, 9, 22].\n\nThe Wright-Fisher model is remarkably versatile as it can be adjusted to many scenarios by the use of effective model parameters: An effective population size, an effective mutation rate and effective selection coefficients. But, crucially, these re-parameterizations cannot account for extremely skewed family size distributions. While remarkably skewed family distributions occur in some natural populations [15], they routinely arise in microbial populations that combine exponential growth with recurrent mutations. This was first highlighted by Luria and Delbruck [26], who noticed that mutations that occur early in an exponential growth process will produce an exceptionally large number of descendants. The distribution of such mutational \"jackpot\" events has a particular power law tail in well-mixed population, as is briefly explained in Fig. 1A. Simplest models of continual evolution [28] and related models of traveling waves [36] can be viewed, on a coarse-grained level, as repeatedly sampling from this jackpot distribution. (The number of draws and the characteristic resampling time scale varies with the model.) It is by now well-established that the ensuing genealogies are described by a particular multiple-merger coalescent [7, 8, 13, 29, 33-35] first identified by Bolthausen and Sznitman [5].\n\nO_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=116 SRC=\"FIGDIR/small/182519_fig1.gif\" ALT=\"Figure 1\">\nView larger version (16K):\norg.highwire.dtl.DTLVardef@d391e7org.highwire.dtl.DTLVardef@ff4eaorg.highwire.dtl.DTLVardef@198495aorg.highwire.dtl.DTLVardef@f7b58e_HPS_FORMAT_FIGEXP M_FIG O_FLOATNOFIG. 1:C_FLOATNO A) Illustration of mutational jackpot events, first studied by Luria and Delbriick. Consider the growth of a well-mixed population of microbes starting from a single cell (ignore death). A mutation that occurs in the jth cell division will have a final frequency of about {approx} 1/j (j = 4 in the illustration) and thus a \"family size\" of u = N/j. Hence, the probability Pr[U > u] to reach an even larger family size U is equal to the probability {approx} j/N = 1/u that the mutation occurs prior to the nth cell division. The probability density to acquire a family size u therefore exhibits a power law tail p(u) {propto} u-2. (Our argument ignores the stochasticity in cell division events, which however does not change the power law exponent.) B) The blue line indicates the probability Pr[U > u] that the family size U of a mutation is larger than u. The largest family size u* in a sample of N jackpot events should typically be of order N because the probability of sampling an even larger event is 1/n (dashed lines). A typical n-sample, therefore, has a mean family size of order log(n), which is obtained upon truncating the family size distribution at u*. It turns out that this effect generates a selection-like bias favoring majority alleles, which is compensated by rare sampling events that favor minority alleles.\n\nC_FIG\n\nWhile extensions of the Wright-Fisher diffusion process to capture skewed offspring numbers have been formally constructed [2, 3, 14, 20], also including selection and mutations [1, 10, 11, 16, 18], we still lack explicit finite time predictions for the probability distribution of allele frequency trajectories. Our goal here is to fill this gap for the particular case of the Luria-Delbriick jackpot distribution, by characterizing the allele frequency process in such a way that it can be easily generalized, intuitively understood and integrated in time.

evolutionary biology

The SMuSh pathway is essential for survival during growth-induced compressive mechanical stress

Cells that proliferate within a confined environment build up mechanical compressive stress. For example, mechanical pressure emerges in the naturally space-limited tumor environment. However, little is known about how cells sense and respond to mechanical compression. We developed microfluidic bioreactors to enable the investigation of the effects of compressive stress on the growth of the genetically tractable model organism Saccharomyces cerevisiae. We used this system to determine that compressive stress is partly partly sensed through a module consisting of the mucin Msb2, and the cell wall protein Sho1, which act together as a sensor module in one of the two major osmosensing pathways in budding yeast. This signal is transmitted via the MAPKKK kinase Ste11. Thus, we term this mechanosensitive pathway the SMuSh pathway, for Ste11 through Mucin / Sho1 pathway. The SMuSh pathway delays cells in the G1 phase of the cell cycle and improves cell survival in response to growth-induced pressure. We also found that the Cell Wall Integrity (CWI) pathway contributes to the response to mechanical compressive stress. These latter results are confirmed in complimentary experiments in the accompanying manuscript from Mishra et al. When both the SMuSh and the CWI pathways are deleted, cells fail to adapt to compressive stress and all cells lyse at relatively low pressure when grown in confinement. Thus, we define a network that is essential for cell survival during growth under pressure. We term this new mechanosensory system the SCWISh (Survival through the CWI and SMuSh) network.\n\nSignificance StatementGrowth in confined environments leads to the build up of compressive mechanical stresses, which are relevant to diverse fields, from cancer to microbiology. In contrast to tensile stress, little is known about the molecular integration of compressive stresses. In this study, we elucidate the SMuSh pathway, which, together with the Cell Wall Integrity pathway, is essential for viability of the budding yeast S. cerevisiae when growing under mechanical pressure. Pressure-sensing requires the transmembrane mucin, Msb2, which is linked to the actin cortex. Our result raises the intriguing question of whether mucins, widely conserved in eukaryotes and frequently misregulated in cancers, might sense compressive stresses in other organisms, including humans.

cell biology

Mechanical interactions in bacterial colonies and the surfing probability of beneficial mutations

Bacterial conglomerates such as biofilms and microcolonies are ubiquitous in nature and play an important role in industry and medicine. In contrast to well-mixed, diluted cultures routinely used in microbial research, bacteria in a microcolonv interact mechanically with one another and with the substrate to which they are attached. Despite their ubiquity, little is known about the role of such mechanical interactions on growth and biological evolution of microbial populations. Here we use a computer model of a microbial colony of rod-shaped cells to investigate how physical interactions between cells determine their motion in the colony, this affects biological evolution. We show that the probability that a faster-growing mutant \"surfs\" at the colonys frontier and creates a macroscopic sector depends on physical properties of cells (shape, elasticity, friction). Although all these factors contribute to the surfing probability in seemingly different ways, they all ultimately exhibit their effects by altering the roughness of the expanding frontier of the colony and the orientation of cells. Our predictions are confirmed by experiments in which we measure the surfing probability for colonies of different front roughness. Our results show that physical interactions between bacterial cells play an important role in biological evolution of new traits, and suggest that these interaction may be relevant to processes such as de novo evolution of antibiotic resistance.

evolutionary biology

Minimal-assumption inference from population-genomic data

Samples of multiple complete genome sequences contain vast amounts of information about the evolutionary history of populations, much of it in the associations among polymorphisms at different loci. Current methods that take advantage of this linkage information rely on models of recombination and coalescence, limiting the sample sizes and populations that they can analyze. We introduce a method, Minimal-Assumption Genomic Inference of Coalescence (MAGIC), that reconstructs key features of the evolutionary history, including the distribution of coalescence times, by integrating information across genomic length scales without using an explicit model of recombination, demography or selection. Using simulated data, we show that MAGICs performance is comparable to PSMC on single diploid samples generated with standard coalescent and recombination models. More importantly, MAGIC can also analyze arbitrarily large samples and is robust to changes in the coalescent and recombination processes. Using MAGIC, we show that the inferred coalescence time histories of samples of multiple human genomes exhibit inconsistencies with a description in terms of an effective population size based on single-genome data.

evolutionary biology

A simple molecular mechanism explains multiple patterns of cell-size regulation

Increasingly accurate and massive data have recently shed light on the fundamental question of how cells maintain a stable size trajectory as they progress through the cell cycle. Microbes seem to use strategies ranging from a pure sizer, where the end of a given phase is triggered when the cell reaches a critical size, to pure adder, where the cell adds a constant size during a phase. Yet the biological origins of the observed spectrum of behavior remain elusive. We analyze a molecular size-control mechanism, based on experimental data from the yeast S. cerevisiae, that gives rise to behaviors smoothly interpolating between adder and sizer. The size-control is obtained from the titration of a repressor protein by an activator protein that accumulates more rapidly with increasing cell size. Strikingly, the size-control is composed of two different regimes: for small initial cell size, the size-control is a sizer, whereas for larger initial cell size, is is an imperfect adder. Our model thus indicates that the adder and critical size behaviors may just be different dynamical regimes of a single simple biophysical mechanism.

biophysics