Schrödinger Dynamics and Berry Phase of Undulatory Locomotion.

Spectral mode representations play an essential role in various areas of physics, from quantum mechanics to fluid turbulence, but they are not yet extensively used to characterize and describe the behavioral dynamics of living systems. Here, we show that mode-based linear models inferred from experimental live-imaging data can provide an accurate low-dimensional description of undulatory locomotion in worms, centipedes, robots, and snakes. By incorporating physical symmetries and known biological constraints into the dynamical model, we find that the shape dynamics are generically governed by Schrödinger equations in mode space. The eigenstates of the effective biophysical Hamiltonians and their adiabatic variations enable the efficient classification and differentiation of locomotion behaviors in natural, simulated, and robotic organisms using Grassmann distances and Berry phases. While our analysis focuses on a widely studied class of biophysical locomotion phenomena, the underlying approach generalizes to other physical or living systems that permit a mode representation subject to geometric shape constraints.

Observing and Quantifying Fluorescent Reporters.

Genetically encoded fluorescent reporters take advantage of C. elegans' transparency to allow non-invasive, in vivo observation, and recording of physiological processes in intact animals. Here, we discuss the basic microscope components required to observe, image, and measure fluorescent proteins in live animals for students and researchers who work with C. elegans but have limited experience with fluorescence imaging and analysis.

Three-Dimensional Fruit Tissue Habitats for Culturing Caenorhabditis elegans.

Environmental factors influence many traits of biological interest, but reproducing an animal's natural habitat in a controlled laboratory environment is challenging. Environmental enrichment-adding complexity to the usually simplistic conditions under which laboratory animals are raised-offers a potential tool for better understanding biological traits while maintaining controlled laboratory conditions. For the model nematode Caenorhabditis elegans, the contrast between the natural environment and the laboratory conditions in which they are raised is enormous. Although several methods have been developed in an effort to complexify C. elegans laboratory conditions, there is still a need for an enriched controlled laboratory habitat in which C. elegans can be raised over several generations, the bacterial food availability is similar to that in traditional agar plates, and the animals are crawling as opposed to swimming or burrowing. To this end, we describe here a standardized protocol for creating controlled, reproducible, three-dimensional environments for multigenerational maintenance of C. elegans in the laboratory. These environments are derived from decellularized apple hypanthium tissue and have bacterial food uniformly distributed throughout. We also describe how traditional C. elegans methods of collecting synchronized eggs, cleaning contaminated stocks, and collecting animal populations are adapted to our scaffold environment. These methods can be adapted to host different bacteria or bacterial populations, and the resulting scaffolds can be used in a range of experimental designs for behavioral and phenotypical studies in C. elegans and other nematodes. © 2021 The Authors. Current Protocols published by Wiley Periodicals LLC. Basic Protocol 1: Decellularization and storage of apple tissue Basic Protocol 2: Preparation of plates from decellularized apple scaffolds Basic Protocol 3: Synchronization of eggs or animals and cleaning contaminated stocks from scaffold plates Alternate Protocol: Collection of non-synchronized larvae and adults from scaffold plates.

A three-dimensional habitat for C. elegans environmental enrichment.

As we learn more about the importance of gene-environment interactions and the effects of environmental enrichment, it becomes evident that minimalistic laboratory conditions can affect gene expression patterns and behaviors of model organisms. In the laboratory, Caenorhabditis elegans is generally cultured on two-dimensional, homogeneous agar plates abundantly covered with axenic bacteria culture as a food source. However, in the wild, this nematode thrives in rotting fruits and plant stems feeding on bacteria and small eukaryotes. This contrast in habitat complexity suggests that studying C. elegans in enriched laboratory conditions can deepen our understanding of its fundamental traits and behaviors. Here, we developed a protocol to create three-dimensional habitable scaffolds for trans-generational culture of C. elegans in the laboratory. Using decellularization and sterilization of fruit tissue, we created an axenic environment that can be navigated throughout and where the microbial environment can be strictly controlled. C. elegans were maintained over generations on this habitat, and showed a clear behavioral bias for the enriched environment. As an initial assessment of behavioral variations, we found that dauer populations in scaffolds exhibit high-frequency, complex nictation behavior including group towering and jumping behavior.

Environmental Programming of Adult Foraging Behavior in C. elegans.

Foraging strategies should be tuned to the expected distribution of resources in the environment. Tuning can occur over generations and lead to genetic differences in innate foraging behavior or over shorter timescales within an individual's lifespan. Both genetically encoded and experience-based strategies are implemented by neural circuits that respond to environmental cues and track internal states. Caenorhabditis elegans exhibit both between-strain genetic differences and within-strain plasticity in foraging. In individuals, changes in foraging are usually short term and based on recent experience. Here, we tested whether developmental experience could permanently alter foraging. We found that, in most wild strains, early-life starvation led to "cautious" foraging strategies, in which exploration is reduced, and these behavioral changes are associated with altered dynamics in a locomotory circuit. Possessing either the derived (domestication-associated) or ancestral allele of the neuroglobin glb-5 determines foraging plasticity. Overall, we show that C. elegans exhibit adaptive developmental plasticity that affects multiple aspects of foraging behavior and leads to changes in a core navigation circuit and that innate foraging traits and plasticity in those traits are genetically separable. VIDEO ABSTRACT.

Microglial activation induces neuronal death in Chandipura virus infection.

Neurotropic viruses induce neurodegeneration either directly by activating host death domains or indirectly through host immune response pathways. Chandipura Virus (CHPV) belonging to family Rhabdoviridae is ranked among the emerging pathogens of the Indian subcontinent. Previously we have reported that CHPV induces neurodegeneration albeit the root cause of this degeneration is still an open question. In this study we explored the role of microglia following CHPV infection. Phenotypic analysis of microglia through lectin and Iba-1 staining indicated cells were in an activated state post CHPV infection in cortical region of the infected mouse brain. Cytokine Bead Array (CBA) analysis revealed comparatively higher cytokine and chemokine levels in the same region. Increased level of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), Nitric Oxide (NO) and Reactive Oxygen species (ROS) in CHPV infected mouse brain indicated a strong inflammatory response to CHPV infection. Hence it was hypothesized through our analyses that this inflammatory response may stimulate the neuronal death following CHPV infection. In order to validate our hypothesis supernatant from CHPV infected microglial culture was used to infect neuronal cell line and primary neurons. This study confirmed the bystander killing of neurons due to activation of microglia post CHPV infection.

The amyotrophic lateral sclerosis 8 protein, VAP, is required for ER protein quality control.

A familial form of Amyotrophic lateral sclerosis (ALS8) is caused by a point mutation (P56S) in the vesicle-associated membrane protein associated protein B (VapB). Human VapB and Drosophila Vap-33-1 (Vap) are homologous type II transmembrane proteins that are localized to the ER. However, the precise consequences of the defects associated with the P56S mutation in the endoplasmic reticulum (ER) and its role in the pathology of ALS are not well understood. Here we show that Vap is required for ER protein quality control (ERQC). Loss of Vap in flies shows various ERQC associated defects, including protein accumulation, ER expansion, and ER stress. We also show that wild type Vap, but not the ALS8 mutant Vap, interacts with a lipid-binding protein, Oxysterol binding protein (Osbp), and that Vap is required for the proper localization of Osbp to the ER. Restoring the expression of Osbp in the ER suppresses the defects associated with loss of Vap and the ALS8 mutant Vap. Hence, we propose that the ALS8 mutation impairs the interaction of Vap with Osbp, resulting in hypomorphic defects that might contribute to the pathology of ALS8.