734 research outputs found

    Age structure landscapes emerge from the equilibrium between aging and rejuvenation in bacterial populations.

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    The physiological asymmetry between daughters of a mother bacterium is produced by the inheritance of either old poles, carrying non-genetic damage, or newly synthesized poles. However, as bacteria display long-term growth stability leading to physiological immortality, there is controversy on whether asymmetry corresponds to aging. Here we show that deterministic age structure landscapes emerge from physiologically immortal bacterial lineages. Through single-cell microscopy and microfluidic techniques, we demonstrate that aging and rejuvenating bacterial lineages reach two distinct states of growth equilibria. These equilibria display stabilizing properties, which we quantified according to the compensatory trajectories of continuous lineages throughout generations. Finally, we show that the physiological asymmetry between aging and rejuvenating lineages produces complex age structure landscapes, resulting in a deterministic phenotypic heterogeneity that is neither an artifact of starvation nor a product of extrinsic damage. These findings indicate that physiological immortality and cellular aging can both be manifested in single celled organisms

    Cell aging preserves cellular immortality in the presence of lethal levels of damage.

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    Cellular aging, a progressive functional decline driven by damage accumulation, often culminates in the mortality of a cell lineage. Certain lineages, however, are able to sustain long-lasting immortality, as prominently exemplified by stem cells. Here, we show that Escherichia coli cell lineages exhibit comparable patterns of mortality and immortality. Through single-cell microscopy and microfluidic techniques, we find that these patterns are explained by the dynamics of damage accumulation and asymmetric partitioning between daughter cells. At low damage accumulation rates, both aging and rejuvenating lineages retain immortality by reaching their respective states of physiological equilibrium. We show that both asymmetry and equilibrium are present in repair mutants lacking certain repair chaperones, suggesting that intact repair capacity is not essential for immortal proliferation. We show that this growth equilibrium, however, is displaced by extrinsic damage in a dosage-dependent response. Moreover, we demonstrate that aging lineages become mortal when damage accumulation rates surpass a threshold, whereas rejuvenating lineages within the same population remain immortal. Thus, the processes of damage accumulation and partitioning through asymmetric cell division are essential in the determination of proliferative mortality and immortality in bacterial populations. This study provides further evidence for the characterization of cellular aging as a general process, affecting prokaryotes and eukaryotes alike and according to similar evolutionary constraints

    Ancient pigs reveal a near-complete genomic turnover following their introduction to Europe

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    Archaeological evidence indicates that pig domestication had begun by ∼10,500 y before the present (BP) in the Near East, and mitochondrial DNA (mtDNA) suggests that pigs arrived in Europe alongside farmers ∼8,500 y BP. A few thousand years after the introduction of Near Eastern pigs into Europe, however, their characteristic mtDNA signature disappeared and was replaced by haplotypes associated with European wild boars. This turnover could be accounted for by substantial gene flow from local European wild boars, although it is also possible that European wild boars were domesticated independently without any genetic contribution from the Near East. To test these hypotheses, we obtained mtDNA sequences from 2,099 modern and ancient pig samples and 63 nuclear ancient genomes from Near Eastern and European pigs. Our analyses revealed that European domestic pigs dating from 7,100 to 6,000 y BP possessed both Near Eastern and European nuclear ancestry, while later pigs possessed no more than 4% Near Eastern ancestry, indicating that gene flow from European wild boars resulted in a near-complete disappearance of Near East ancestry. In addition, we demonstrate that a variant at a locus encoding black coat color likely originated in the Near East and persisted in European pigs. Altogether, our results indicate that while pigs were not independently domesticated in Europe, the vast majority of human-mediated selection over the past 5,000 y focused on the genomic fraction derived from the European wild boars, and not on the fraction that was selected by early Neolithic farmers over the first 2,500 y of the domestication process

    The Impact of Social Context on Preschoolers’ Flexibility

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    The current study investigates whether social interaction without communication between partners may influence preschoolers’ flexibility. Fifty-three 5 year old Singaporean children were randomly assigned to three conditions of a block sorting task (Fawcett & Garton, 2005): playing individually, cooperating with another player, and competing against another player. To control for individual differences, before the block sorting task children were given four cognitive tasks testing vocabulary, short-term memory, and executive function, as well as two affective scales on mood and motivation. Separate one-way Analysis of Variance (ANOVA) showed that although they performed the same on the cognitive tasks and the affective measures, children in the competition condition sorted blocks along significantly more dimensions compared to children in the individual condition. These results suggest that preschoolers’ flexibility is sensitive to social contexts

    Minicells as a Damage Disposal Mechanism in Escherichia coli

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    Many bacteria produce small, spherical minicells that lack chromosomal DNA and therefore are unable to proliferate. Although minicells have been used extensively by researchers as a molecular tool, nothing is known about why bacteria produce them. Here, we show that minicells help Escherichia coli cells to rid themselves of damaged proteins induced by antibiotic stress. By comparing the survival and growth rates of wild-type strains with the E. coliΔminC mutant, which produces excess minicells, we found that the mutant was more resistant to streptomycin. To determine the effects of producing minicells at the single-cell level, we also tracked the growth of ΔminC lineages by microscopy. We were able to show that the mutant increased the production of minicells in response to a higher level of the antibiotic. When we compared two sister cells, in which one produced minicells and the other did not, the daughters of the former had a shorter doubling time at this higher antibiotic level. Additionally, we found that minicells were more likely produced at the mother's old pole, which is known to accumulate more aggregates. More importantly, by using a fluorescent IbpA chaperone to tag damage aggregates, we found that polar aggregates were contained by and ejected with the minicells produced by the mother bacterium. These results demonstrate for the first time the benefit to bacteria for producing minicells.IMPORTANCE Bacteria have the ability to produce minicells, or small spherical versions of themselves that lack chromosomal DNA and are unable to replicate. A minicell can constitute as much as 20% of the cell's volume. Although molecular biology and biotechnology have used minicells as laboratory tools for several decades, it is still puzzling that bacteria should produce such costly but potentially nonfunctional structures. Here, we show that bacteria gain a benefit by producing minicells and using them as a mechanism to eliminate damaged or oxidated proteins. The elimination allows the bacteria to tolerate higher levels of stress, such as increasing levels of streptomycin. If this mechanism extends from streptomycin to other antibiotics, minicell production could be an overlooked pathway that bacteria are using to resist antimicrobials

    Amblyopia and Strabismus in young Singaporean children

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