Biology subjects

Hinz, A.

Publications and source records attributed to Hinz, A..

4 recordsLinked to original sources

bioRxiv2025

Investigating Cobalt Corrosion Mechanisms in a Phenazine Producing Bacterium

Microbially-induced corrosion (MIC) has been well-studied in the context of damage to iron-bearing infrastructure, where microbes can solubilize solid elemental iron using redox-active metabolites such as phenazines. Whether such pathways can solubilize economically-critical cobalt remains poorly understood. We hypothesized that secondary metabolites produced by the model bacterium Pseudomonas chlororaphis subspecies aureofaciens associated with MIC of iron could corrode cobalt by oxidation (i.e., phenazines) or by acting as a ligand (i.e., cyanide). One-week incubations using live cells supplied with Co(0) wires led to 20-30% cobalt mass losses and [~]2200 {micro}M Co(2+) recovered in solution, which was at least 3-fold higher than filtered cultures and sterile medium controls. Removing the capacity for cells to produce phenazines and cyanide showed similar corrosion compared to wild type cells and phenazine standards did not corrode cobalt, ruling these metabolites out as contributors to MIC. Further experiments testing whether metabolite mixtures devoid of phenazines could corrode Co(0) in the presence and absence of oxygen confirmed that atmospheric oxygen initiates Co(0) oxidation, and that unidentified cell-derived metabolites drive MIC forward by keeping Co(2+) from precipitating as oxides that form a passivation layer on the wire surface. This revised mechanistic explanation underscores the importance of considering how abiotic redox cycling and cellular metabolites that solubilize metals interact in the MIC of non-ferrous metals. Identifying the biosynthetic pathways involved in solubilizing cobalt will be key to reframing MIC as more than an environmental concern and optimizing sustainable cobalt recovery strategies for solid waste that rely on naturally-occurring microbial metabolites. ImportanceCharacterizing microbially-induced corrosion mechanisms for cobalt is important for predicting the fate of critical metals in the environment and optimizing sustainable strategies for cobalt reclamation from electronic waste. This study uses the model bacterium Pseudomonas chlororaphis subspecies aureofaciens to test if redox-active phenazines and the metal-binding metabolite cyanide can corrode elemental cobalt. We repeatedly observed that live cells corroded cobalt, but that corrosion did not rely on phenazines or cyanide. Instead, our results show that oxygen oxidized elemental cobalt and unidentified metabolites keep cobalt ions in solution to limit cobalt oxide precipitation and drive the corrosion reaction forward. Our study reinforces the need to consider connections between abiotic and biotic reactions in the corrosion of metals other than iron. Understanding these mechanisms is critical to reframing microbial corrosion as a sustainable approach for metal recovery and our study makes the case that it is possible for the critical metal cobalt.

microbiology↗

bioRxiv2023

Unpredictability of the fitness effects of antimicrobial resistance mutations across environments in Escherichia coli

The evolution of antimicrobial resistance (AMR) in bacteria is a major public health concern. When resistant bacteria are highly prevalent in microbial populations, antibiotic restriction protocols are often implemented to reduce their spread. These measures rely on the existence of deleterious fitness effects (i.e., costs) imposed by AMR mutations during growth in the absence of antibiotics. According to this assumption, resistant strains will be outcompeted by susceptible strains that do not pay the cost during the period of restriction. Hence, the success of a given intervention depends on the magnitude and direction of fitness effects of mutations, which can vary depending on the genetic and environmental context. However, the fitness effects of AMR mutations are generally studied in laboratory reference strains and estimated in a limited number of environments, usually a standard laboratory growth medium. In this study, we systematically measure how three sources of variation impact the fitness effects of AMR mutations: the type of resistance mutation, the genetic background of the host, and the growth environment. We demonstrate that while AMR mutations are generally costly in antibiotic-free environments, their fitness effects vary widely and depend on complex interactions between the AMR mutation, genetic background, and environment. We test the ability of the Rough Mount Fuji genotype-fitness model to reproduce the empirical data in simulation. We identify model parameters that reasonably capture the variation in fitness effects due to genetic variation. However, the model fails to accommodate variation when considering multiple growth environments. Overall, this study reveals a wealth of variation in the fitness effects of resistance mutations owing to genetic background and environmental conditions, that will ultimately impact their persistence in natural populations. Authors AbstractThe emergence and spread of antimicrobial resistance in bacterial populations poses a continuing threat to our ability to successfully treat bacterial infections. During exposure to antibiotics, resistant microbes outcompete susceptible ones, leading to increases in prevalence. This competitive advantage, however, can be reversed in antibiotic-free environments, due to deleterious fitness effects imposed by resistance determinants, a concept referred to as the cost of resistance. The extent of these fitness effects is an important factor governing the prevalence of resistance in natural populations. However, predicting the fitness effects of resistance mutations is challenging, since their magnitude can change depending on the genetic background in which the mutation arose and the environmental context. Comprehensive data on these sources of variation is lacking, and we address this gap by determining the fitness effects of resistance mutations introduced in a range of Escherichia coli clinical isolates, measured in different antibiotic-free environments. Our results reveal wide variation in the fitness effects, driven by irreducible interactions between resistance mutations, genetic backgrounds, and growth environments. We evaluate the performance of a fitness landscape model to reproduce the data in simulation, highlight its strengths and weaknesses, and call for improvements to accommodate these important sources of variation.

evolutionary biology↗

bioRxiv2022

Mortality without springing a leak: Locust gut epithelia do not become more permeable to fluorescent dextran and bacteria in the cold

The insect gut, which plays a role in ion and water balance, has been shown to leak solutes in the cold. Cold stress can also activate insect immune systems, but it is unknown if the leak of the gut microbiome is a possible immune trigger in the cold. We developed a novel feeding protocol to load the gut of locusts (Locusta migratoria) with fluorescent bacteria before exposing them to -2{degrees}C for up to 48 h. No bacteria were recovered from the hemolymph of cold-exposed locusts, regardless of exposure duration. To examine this further, we used an ex vivo gut sac preparation to re-test cold-induced fluorescent FITC-dextran leak across the gut and found no increased rate of leak. These results question not only the validity of FITC-dextran as a marker of paracellular barrier permeability in the gut, but also to what extent the insect gut becomes leaky in the cold.

physiology↗

bioRxiv2019

The distribution of fitness effects among synonymous mutations in a gene under selection

The fitness effects of synonymous mutations, nucleotide changes that do not alter the encoded amino acid, have often been assumed to be neutral, but a growing body of evidence suggests otherwise. We used site-directed mutagenesis coupled with direct measures of competitive fitness to estimate the distribution of fitness effects among synonymous mutations for a gene under selection. Synonymous mutations had highly variable fitness effects, both deleterious and beneficial, resembling those of nonsynonymous mutations in the same gene. This variation in fitness was underlain by changes in transcription linked to the creation of internal promoter sites. A positive correlation between fitness and the presence of synonymous substitutions across a phylogeny of related Pseudomonads suggests these mutations may be common in nature. Taken together, our results provide the most compelling evidence to date that synonymous mutations with non-neutral fitness effects may in fact be commonplace.

evolutionary biology↗