Citizen (community) science platforms have become a crucial aspect of involving the public in scientific research. The platform Zooniverse particularly has grown to include a wide range of participants in the scientific community. Though there is a substantial amount of literature surrounding the efficacy of community science platforms, relatively few studies tackle applications in undergraduate education. This study investigates undergraduate student engagement with Zooniverse. Utilizing Zooniverse, participants analyzed the flowering of North Texas prairie species. Primary objectives include documenting the accuracy and speed of student identifications and comparing potential differences between historical botanical specimen images provided by the Botanical Research Institute of Texas and images collected from iNaturalist. These findings will help inform the usage of community science platforms in undergraduate education spaces and more particularly for non-science majors.

As the number of antibiotics in development dwindles and antibiotic resistance continues to rise,
there is a need for novel, non-traditional antibiotics such as zinc oxide nanoparticles (ZnO NPs).
While the broad-spectrum antimicrobial properties are well established, the mechanism of action
is still unknown. Previous work has proposed that reactive oxygen species (ROS), toxic Zn2+ ions,
and electrostatic interactions with the cell envelope may be implicated in the mechanism. To
evaluate which of these mechanisms are involved, we characterized the physical and genetic
properties that confer resistance to ZnO NPs in three novel ZnO resistant strains of
Staphylococcus aureus (ZnOR). These strains possess comparable growth rates and are at least
four times more resistant than the parental strain against ZnO NPs acquired from multiple
sources. This suggests that all ZnO NPs, regardless of morphology, size, or method of synthesis
share a mechanism of action. We found that cell charge, measured by cytochrome c, was not
different between the parental and resistant strains, indicating that electrostatic interactions
with the membrane are not involved in the mechanism. Additionally, the ZnOR strains shared a
similar susceptibility to H2O2, a ROS commonly suggested to be generated by ZnO. We have also
found that internalization and physical contact with the bacterial envelope are not necessary for
ZnO mediated growth inhibition suggesting that ZnO produces a soluble species that is
responsible for the antibacterial action. Future work includes sequencing the genome of the
parental and ZnOR strains to identify mutations that led to gain of resistance.

Bacillus anthracis is the causative agent of the fatal disease anthrax, and its virulence is of great interest due to its potential as a biological weapon. B. anthracis causes disease by both escaping immune defenses and acquiring nutrients. A necessary nutrient that pathogens must acquire from its host is iron. To discover novel genes essential for iron acquisition, we screened transposon mutants in iron-deficient media with hemoglobin as the sole source of iron. We further prioritized the mutants discovered in our in vitro screen by assessing for attenuated virulence using our in vivo G. mellonella infection model. We found one mutant that has a disruption in the first gene of a two-gene operon containing putative dUTPase and aminopeptidase genes known as 9F12 Tn. Neither of these genes have been previously linked to iron acquisition. To confirm the role of the dUTPase gene in the observed 9F12 Tn phenotype, we created an independent insertional mutant in the dUTPase gene (dUTPase IM). We found that both of our mutants, 9F12 Tn and dUTPase IM, could not use hemoglobin as a source of iron. We also found that G. mellonella injected with 9F12 Tn and dUTPase IM had higher survival rates than those injected with the parent strain. Our results indicate that the dUTPase gene is necessary for iron-acquisition and virulence in B. anthracis. This study furthers our understanding of iron acquisition in a bacterial pathogen and increases our knowledge of how B. anthracis causes disease.

Bacillus anthracis is a gram-positive bacterium that causes the deadly anthrax disease. ClpX is a subunit of ClpXP protease that is known to be essential in virulence as well as providing resistance to cell-envelope targeting antibiotics such as penicillin, daptomycin, and the antimicrobial peptide LL-37. While clpX is critical for virulence in B. anthracis, it is unlikely to be directly mediating the effect. Hence, our lab investigated the genes that are differentially expressed in the ΔclpX mutant compared to the wild type B. anthracis through microarray analysis. We found 119 genes that were highly differentially expressed in the ΔclpX mutant. In this study, we focused on two genes sigM and glpF, which are downregulated in the ΔclpX mutant, because sigM and glpF confer resistance to cell-wall targeting antibiotics in the closely related gram-positive bacterial species, Bacillus subtilis and Staphylococcus aureus respectively. We wanted to determine whether loss of sigM and glpF will lead to similar phenotypes as loss of clpX in B. anthracis Sterne. We found that sigM mutant is more susceptible to penicillin and daptomycin, although in a growth phase dependent manner, but glpF mutant is not. Future studies will examine the susceptibility of these mutants to LL-37 and other stressors such as acid and heat stress. Complementation of these mutants will serve to further support the importance of these genes for the roles we examined. This research will aid in understanding the mechanism of antibiotic resistance and virulence in the ClpX regulatory network in B. anthracis.

Salmon hatcheries are widely used across the Pacific Northwest to enhance fisheries and supplement declining wild populations. However, substantial evidence suggests that hatchery fish have reduced fitness compared to their wild counterparts. Domestication selection, or adaptation to the hatchery environment, poses a potential risk to wild populations if introgression between hatchery and wild fish occurs. While few studies have investigated domestication selection on a genomic level, none have done so in parallel across multiple hatchery-wild population pairs. In this study, we examined three separate hatchery populations of Chinook salmon, Oncorhynchus tshawytscha, and their corresponding wild progenitor populations using low-coverage whole genome sequencing. We sequenced 192 individuals from populations across Southeast Alaska and estimated genotype likelihoods at over six million loci. Each hatchery population, which was reared in a hatchery for approximately seven generations, was then compared to its wild progenitor population using multiple metrics of genomic divergence. While evaluating population-level genomic differentiation (FST), we discovered numerous outlier peaks in each hatchery-wild pair, although no outliers were shared across the three comparisons. Further analyses indicated that these relatively small (5 – 10 kilobase) peaks are likely due to genetic hitchhiking on hatchery-selected alleles, though the effects of these peaks on fitness are unknown. Overall, our genome-wide analyses demonstrate that domestication selection is prevalent in all hatchery facilities, but the genetic pathways differ across populations, possibly due to a polygenic basis of fitness related traits. These results provide fine-scale genetic evidence for domestication and highlight the need to assess if certain management practices, such as integration of wild broodstock, can universally mitigate genetic risks despite multiple pathways of domestication.