An active learning card game to teach microbial pathogenesis to undergraduate biology majors.

Interactive classroom activities are an effective way to reinforce knowledge and promote student engagement. In this paper, we introduce the Pathogenesis Card Game (PCG), an innovative card game that engages students in a battle between microbial pathogens and the host immune system. Each student is given a set of cards that consist of either common host defenses or common pathogen evasion strategies. In pairs, students play a host defense card versus a pathogenesis card. Host defense cards include neutralize (antibody production), eat (phagocytosis), and destroy (degranulation). Pathogenesis cards present evasive strategies including mimic (molecular mimicry), escape (hemolysin production), hide (polysaccharide capsule), block (antioxidant defense), cut (protease secretion), and disguise (antigenic variation). Students develop a mastery of microbial pathogenesis through active gameplay by deliberating the outcome of each unique host-pathogen interaction. Furthermore, they learn the role of cells in the immune system and how pathogens can evade these immune defenses. PCG was piloted in a 300-level introductory microbiology course for 22 undergraduate students, comprising primarily biology and nursing majors. Both quantitative and qualitative student evaluations of the activity strongly suggest that PCG is an engaging, effective, and useful way to teach microbial pathogenesis. This activity provides a 60-minute lesson plan and corresponding materials that can be used to facilitate the introduction of pathogenesis to a typical undergraduate microbiology course. PCG offers instructors a framework to teach microbial pathogenesis and gives students the opportunity to construct their own knowledge about pathogen immune evasion in an engaging and interactive way.

McaA and McaB control the dynamic positioning of a bacterial magnetic organelle.

Magnetotactic bacteria are a diverse group of microorganisms that use intracellular chains of ferrimagnetic nanocrystals, produced within magnetosome organelles, to align and navigate along the geomagnetic field. Several conserved genes for magnetosome formation have been described, but the mechanisms leading to distinct species-specific magnetosome chain configurations remain unclear. Here, we show that the fragmented nature of magnetosome chains in Magnetospirillum magneticum AMB-1 is controlled by genes mcaA and mcaB. McaA recognizes the positive curvature of the inner cell membrane, while McaB localizes to magnetosomes. Along with the MamK actin-like cytoskeleton, McaA and McaB create space for addition of new magnetosomes in between pre-existing magnetosomes. Phylogenetic analyses suggest that McaA and McaB homologs are widespread among magnetotactic bacteria and may represent an ancient strategy for magnetosome positioning.

Empowering Undergraduates to Fight Climate Change with Soil Microbes.

The burning of fossil fuels to meet a growing demand for energy has created a climate crisis that threatens Earth's fragile ecosystems. While most undergraduate students are familiar with solar and wind energy as sustainable alternatives to fossil fuels, many are not aware of a climate solution right beneath their feet-soil-dwelling microbes! Microbial fuel cells (MFCs) harness energy from the metabolic activity of microbes in the soil to generate electricity. Recently, the coronavirus disease 2019 (COVID-19) pandemic transformed the traditional microbiology teaching laboratory into take-home laboratory kits and online modes of delivery, which could accommodate distance learning. This laboratory exercise combined both virtual laboratory simulations and a commercially available MFC kit to challenge undergraduate students to apply fundamental principles in microbiology to real-world climate solutions.

How to rewire the host cell: A home improvement guide for intracellular bacteria.

Intracellular bacterial pathogens have developed versatile strategies to generate niches inside the eukaryotic cells that allow them to survive and proliferate. Making a home inside the host offers many advantages; however, intracellular bacteria must also overcome many challenges, such as disarming innate immune signaling and accessing host nutrient supplies. Gaining entry into the cell and avoiding degradation is only the beginning of a successful intracellular lifestyle. To establish these replicative niches, intracellular pathogens secrete various virulence proteins, called effectors, to manipulate host cell signaling pathways and subvert host defense mechanisms. Many effectors mimic host enzymes, whereas others perform entirely novel enzymatic functions. A large volume of work has been done to understand how intracellular bacteria manipulate membrane trafficking pathways. In this review, we focus on how intracellular bacterial pathogens target innate immune signaling, the unfolded protein response, autophagy, and cellular metabolism and exploit these pathways to their advantage. We also discuss how bacterial pathogens can alter host gene expression by directly modifying histones or hijacking the ubiquitination machinery to take control of several host signaling pathways.

Dynamic Remodeling of the Magnetosome Membrane Is Triggered by the Initiation of Biomineralization.

UNLABELLED: Magnetotactic bacteria produce chains of membrane-bound organelles that direct the biomineralization of magnetic nanoparticles. These magnetosome compartments are a model for studying the biogenesis and subcellular organization of bacterial organelles. Previous studies have suggested that discrete gene products build and assemble magnetosomes in a stepwise fashion. Here, using an inducible system, we show that the stages of magnetosome formation are highly dynamic and interconnected. During de novo formation, magnetosomes first organize into discontinuous chain fragments that are subsequently connected by the bacterial actin-like protein MamK. We also find that magnetosome membranes are not uniform in size and can grow in a biomineralization-dependent manner. In the absence of biomineralization, magnetosome membranes stall at a diameter of ~50 nm. Those that have initiated biomineralization then expand to significantly larger sizes and accommodate mature magnetic particles. We speculate that such a biomineralization-dependent checkpoint for membrane growth establishes the appropriate conditions within the magnetosome to ensure successful nucleation and growth of magnetic particles. IMPORTANCE: Magnetotactic bacteria make magnetic nanoparticles inside membrane-bound organelles called magnetosomes; however, it is unclear how the magnetosome membrane controls the biomineralization that occurs within this bacterial organelle. We placed magnetosome formation under inducible control in Magnetospirillum magneticum AMB-1 and used electron cryo-tomography to capture magnetosomes in their near-native state as they form de novo. An inducible system provided the key evidence that magnetosome membranes grow continuously unless they have not properly initiated biomineralization. Our finding that the size of a bacterial organelle impacts its biochemical function is a fundamental advance that impacts our perception of organelle formation and can inform future attempts aimed at creating designer magnetic particles.

Compartmentalization and organelle formation in bacteria.

A number of bacterial species rely on compartmentalization to gain specific functionalities that will provide them with a selective advantage. Here, we will highlight several of these modes of bacterial compartmentalization with an eye toward describing the mechanisms of their formation and their evolutionary origins. Spore formation in Bacillus subtilis, outer membrane biogenesis in Gram-negative bacteria and protein diffusion barriers of Caulobacter crescentus will be used to demonstrate the physical, chemical, and compositional remodeling events that lead to compartmentalization. In addition, magnetosomes and carboxysomes will serve as models to examine the interplay between cytoskeletal systems and the subcellular positioning of organelles.