The recent exponential increase in the use of engineered nanoparticles (eNPs) means both greater intentional and unintentional exposure of eNPs to microbes. Intentional use includes the use of eNPs as biocides. Unintentional exposure results from the fact that eNPs are included in a variety of commercial products (paints, sunscreens, cosmetics). Many of these eNPs are composed of heavy metals or metal oxides such as silver, gold, zinc, titanium dioxide, and zinc oxide. It is thought that since metallic/metallic oxide NPs impact so many aspects of bacterial physiology that it will difficult for bacteria to evolve resistance to them. This study utilized laboratory experimental evolution to evolve silver nanoparticle (AgNP) resistance in the bacterium Escherichia coli (K12 MG1655), a bacterium that did not harbor any silver resistance elements. After 225 generations of exposure to the AgNP environment, the treatment populations demonstrated greater fitness versus control strains as measured by optical density (OD) and colony forming units (CFU) in the presence of varying concentrations of 10nm citrate-coated silver nanoparticles (AgNP) or silver nitrate (AgNO3). Genomic analysis shows that changes associated with AgNP resistance were already accumulating within the treatment populations by generation 100, and by generation 200 three mutations had swept to high frequency in the AgNP resistance stocks. This study indicates that despite previous claims to the contrary bacteria can easily evolve resistance to AgNPs, and this occurs by relatively simple genomic changes. These results indicate that care should be taken with regards to the use of eNPs as biocides as well as with regards to unintentional exposure of microbial communities to eNPs in waste products.

The history of the scientific enterprise demonstrates that it has supported gender, identity, and racial inequity. Further, its institutions have allowed discrimination, harassment, and personal harm of racialized persons and women. This has resulted in a suboptimal and demographically narrow research and innovation system, a concomitant limited lens on research agendas, and less effective knowledge translation between science and society. We argue that, to reverse this situation, the scientific community must reexamine its values and then collectively embark upon a moonshot-level new agenda for equity. This new agenda should be based upon the foundational value that scientific research and technological innovation should be prefaced upon progress toward a better world for all of society and that the process of how we conduct research is just as important as the results of research. Such an agenda will attract individuals who have been historically excluded from participation in science, but we will need to engage in substantial work to overcome the longstanding obstacles to their full participation. We highlight the need to implement this new agenda via a coordinated systems approach, recognizing the mutually reinforcing feedback dynamics among all science system components and aligning our equity efforts across them.

Antibiotic resistance is a growing health concern. Efforts to control resistance would benefit from an improved ability to forecast when and how it will evolve. Epistatic interactions between mutations can promote divergent evolutionary trajectories, which complicates our ability to predict evolution. We recently showed that differences between genetic backgrounds can lead to idiosyncratic responses in the evolvability of phenotypic resistance, even among closely related Escherichia coli strains. In this study, we examined whether a strain9s genetic background also influences the genotypic evolution of resistance. Do lineages founded by different genotypes take parallel or divergent mutational paths to achieve their evolved resistance states? We addressed this question by sequencing the complete genomes of antibiotic-resistant clones that evolved from several different genetic starting points during our earlier experiments. We first validated our statistical approach by quantifying the specificity of genomic evolution with respect to antibiotic treatment. As expected, mutations in particular genes were strongly associated with each drug. Then, we determined that replicate lines evolved from the same founding genotypes had more parallel mutations at the gene level than lines evolved from different founding genotypes, although these effects were more subtle than those showing antibiotic specificity. Taken together with our previous work, we conclude that historical contingency can alter both genotypic and phenotypic pathways to antibiotic resistance. Significance A fundamental question in evolution is the repeatability of adaptation. Will independently evolving populations respond similarly when facing the same environmental challenge? This question also has important public-health implications related to the growing problem of antibiotic resistance. For example, efforts to control resistance might benefit from accurately predicting mutational paths to resistance. However, this goal is complicated when a lineage’s prior history alters its subsequent evolution. We recently found that differences between genetic backgrounds can lead to unpredictable responses in phenotypic resistance. Here, we report that genetic background can similarly alter genotypic paths to resistance. This historical contingency underscores the importance of accounting for stochasticity, in the past as well as at present, when designing evolutionarily informed treatment strategies.

In 2017 National Science Foundation data revealed that in the United States the professional biological workforce was composed of ~ 69.5% “whites”, 21.3% “Asians”, and only 3% “African American or Blacks” (National Science Foundation, 2017, https://ncsesdata.nsf.gov/doctoratework/2017/html/sdr2017_dst_03.html). There are problems with the categories themselves but without too deep an investigation of these, these percentages are representative of the demography of biology as a whole over the latter portion of the twentieth and beginning of the twenty-first century. However, evolutionary biologists would argue (and correctly so) that the representation of persons of African descent in our field is probably an order of magnitude lower (0.3%). This commentary focuses on the factors that are associated with underrepresentation of African Americans in evolutionary science careers.

Due to the widespread occurrence of multidrug resistant microbes there is increasing interest in the use of novel nanostructured materials as antimicrobials. Specifically, metallic nanoparticles such as silver, copper, and gold have been deployed due to the multiple impacts they have on bacterial physiology. From this, many have concluded that such nanomaterials represent steep obstacles against the evolution of resistance. However, we have already shown that this view is fallacious. For this reason, the significance of our initial experiments are beginning to be recognized in the antimicrobial effects of nanomaterials literature. This recognition is not yet fully understood and here we further explain why nanomaterials research requires a more nuanced understanding of core microbial evolution principles.

Metallic antimicrobial materials are of growing interest due to their potential to control pathogenic and multidrug-resistant bacteria. Yet we do not know if utilizing these materials can lead to genetic adaptations that produce even more dangerous bacterial varieties. Here we utilize experimental evolution to produce strains of Escherichia coli K-12 MG1655 resistant to, the iron analog, gallium nitrate (Ga(NO₃)₃). Whole genome sequencing was utilized to determine genomic changes associated with gallium resistance. Computational modeling was utilized to propose potential molecular mechanisms of resistance. By day 10 of evolution, increased gallium resistance was evident in populations cultured in medium containing a sublethal concentration of gallium. Furthermore, these populations showed increased resistance to ionic silver and iron (III), but not iron (II) and no increase in traditional antibiotic resistance compared with controls and the ancestral strain. In contrast, the control populations showed increased resistance to rifampicin relative to the gallium-resistant and ancestral population. Genomic analysis identified hard selective sweeps of mutations in several genes in the gallium (III)-resistant lines including: fecA (iron citrate outer membrane transporter), insl1 (IS30 tranposase) one intergenic mutations arsC →/→ yhiS; (arsenate reductase/pseudogene) and in one pseudogene yedN ←; (iapH/yopM family). Two additional significant intergenic polymorphisms were found at frequencies > 0.500 in fepD ←/→ entS (iron-enterobactin transporter subunit/enterobactin exporter, iron-regulated) and yfgF ←/→ yfgG (cyclic-di-GMP phosphodiesterase, anaerobic/uncharacterized protein). The control populations displayed mutations in the rpoB gene, a gene associated with rifampicin resistance. This study corroborates recent results observed in experiments utilizing pathogenic Pseudomonas strains that also showed that Gram-negative bacteria can rapidly evolve resistance to an atom that mimics an essential micronutrient and shows the pleiotropic consequences associated with this adaptation. We utilize experimental evolution to produce strains of Escherichia coli K-12 MG1655 resistant to, the iron analog, gallium nitrate (Ga(NO₃)₃). Whole genome sequencing was utilized to determine genomic changes associated with gallium resistance. Computational modeling was utilized to propose potential molecular mechanisms of resistance.