Chalasani Lab

Animal foraging is an essential and evolutionarily conserved behavior that occurs in social and solitary contexts, but the underlying molecular pathways are not well defined. We discover that conserved autism-associated genes (NRXN1(nrx-1), NLGN3(nlg-1), GRIA1,2,3(glr-1), GRIA2(glr-2), and GLRA2,GABRA3(avr-15)) regulate aggregate feeding in C. elegans, a simple social behavior. NRX-1 functions in chemosensory neurons (ADL and ASH) independently of its postsynaptic partner NLG-1 to regulate social feeding. Glutamate from these neurons is also crucial for aggregate feeding, acting independently of NRX-1 and NLG-1. Compared to solitary counterparts, social animals show faster presynaptic release and more presynaptic release sites in ASH neurons, with only the latter requiring nrx-1. Disruption of these distinct signaling components additively converts behavior from social to solitary. Collectively, we find that aggregate feeding is tuned by conserved autism-associated genes through complementary synaptic mechanisms, revealing molecular principles driving social feeding.

Animals with small nervous systems have a limited number of sensory neurons that must encode information from a changing environment. This problem is particularly exacerbated in nematodes that populate a wide variety of distinct ecological niches but only have a few sensory neurons available to encode multiple modalities. How does sensory diversity prevail within this neuronal constraint? To identify the genetic basis for patterning different nervous systems, we demonstrate that sensory neurons in the respond to various salt sensory cues in a manner that is partially distinct from that of the distantly related nematode . By visualizing neuronal activity patterns, we show that contrary to previous expectations based on its genome sequence, the salt responses of are encoded in a left/right asymmetric manner in the bilateral ASE neuron pair. Our study illustrates patterns of evolutionary stability and change in the gustatory system of nematodes.

Neurexins and their canonical binding partners, neuroligins, are localized to neuronal pre-, and post-synapses, respectively, but less is known about their role in driving behaviors. Here, we use the nematode C. elegans to show that neurexin, but not neuroligin, is required for avoiding specific chemorepellents. We find that adults with knockouts of the entire neurexin locus exhibit a strong avoidance deficit in response to glycerol and a weaker defect in response to copper. Notably, the C. elegans neurexin (nrx-1) locus, like its mammalian homologs, encodes multiple isoforms, α and γ. Using isoform-specific mutations, we find that the γ isoform is selectively required for glycerol avoidance. Next, we used transgenic rescue experiments to show that this isoform functions at least partially in the nervous system. We also confirm that the transgenes are expressed in the neurons and observe protein accumulation in neurites. Furthermore, we tested whether these mutants affect the behavioral responses of juveniles. We find that juveniles (4th larval stages) of mutants knocking out the entire locus or the α-isoforms, but not γ-isoform, are defective in avoiding glycerol. These results suggest that the different neurexin isoforms affect chemosensory avoidance behavior in juveniles and adults, providing a general principle of how isoforms of this conserved gene affect behavior across species.

In the wild, are emersed in environments teeming with a veritable menagerie of microorganisms. The cuticular surface serves as a barrier and first point of contact with their microbial environments. In this study, we identify microbes from natural habitats that associate with its cuticle, constituting a simple “skin microbiome.” We rear our animals on a modified CeMbio, mCeMbio, a consortium of ecologically relevant microbes. We first combine standard microbiological methods with an adapted micro skin-swabbing tool to describe the skin-resident bacteria on the surface. Furthermore, we conduct 16S rRNA gene sequencing studies to identify relative shifts in the proportion of mCeMbio bacteria upon surface-sterilization, implying distinct skin- and gut-microbiomes. We find that some strains of bacteria, including sp. JUb101 are primarily found on the nematode skin, while others like JUb19 and MYb71 are predominantly found in the animal’s gut. Finally, we show that this skin microbiome promotes host cuticle integrity in harsh environments. Together, we identify a skin microbiome for the well-studied nematode model and propose its value in conferring host fitness advantages in naturalized contexts.

Animals have evolved to seek, select, and exploit food sources in their environment. Collectively termed foraging, these ubiquitous behaviors are necessary for animal survival. As a foundation for understanding foraging, behavioral ecologists established early theoretical and mathematical frameworks which have been subsequently refined and supported by field and laboratory studies of foraging animals. These simple models sought to explain how animals decide which strategies to employ when locating food, what food items to consume, and when to explore the environment for new food sources. These foraging decisions involve integration of prior experience with multimodal sensory information about the animal’s current environment and internal state. We suggest that the nematode Caenorhabditis elegans is well-suited for a high-resolution analysis of complex goal-oriented behaviors such as foraging. We focus our discussion on behavioral studies highlighting C. elegans foraging on bacteria and summarize what is known about the underlying neuronal and molecular pathways. Broadly, we suggest that this simple model system can provide a mechanistic understanding of decision-making and present additional avenues for advancing our understanding of complex behavioral processes.