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Amino acids (AAs) are essential dietary macronutrients that impact an organism's fitness in a concentration-dependent manner, but the mechanisms mediating AA detection to drive consumption are less clear. In Drosophila, we identified the repertoire of taste cells and receptors that are salient for feeding initiation when flies encounter a glutamate-rich AA peptide mixture, tryptone, using in vivo calcium imaging and the proboscis extension response. We found that tryptone attraction occurs through sweet cells, whereas feeding aversion is mediated through Ionotropic Receptor 94e (IR94e) cells and bitter cells, dependent on concentration. Further, our results corroborate previous findings that IR76b, IR51b, and IR94e detect AAs in specific cell types, even when exposed to a more complex peptide mixture. Additionally, we describe a new role for the appetitive IR56d receptor and bitter gustatory receptors in sensing tryptone. This work establishes a cellular and molecular framework salient for AA and peptide feeding initiation and highlights redundancy in aversive pathways that regulate AA feeding. 

Chemosensory cells across the body of Drosophila melanogaster evaluate the environment to prioritize certain behaviors. Previous mapping of gustatory receptor neurons (GRNs) on the fly labellum identified a set of neurons in L-type sensilla that express Ionotropic Receptor 94e (IR94e), but the impact of IR94e GRNs on behavior remains unclear. We used optogenetics and chemogenetics to activate IR94e neurons and found that they drive mild feeding suppression but enhance egg laying. In vivo calcium imaging revealed that IR94e GRNs respond strongly to certain amino acids, including glutamate, and that IR94e plus co-recep- tors IR25a and IR76b are required for amino acid detection. Furthermore, IR94e mutants show behavioral changes to solutions containing amino acids, including increased consumption and decreased egg laying. Overall, our results suggest that IR94e GRNs on the fly labellum discourage feeding and encourage egg laying as part of an important behavioral switch in response to certain chemical cues. 

Stalk lodging is the event of failure just below the ear or node. The most common failure mode is Brazier (localized) buckling, which occurs consistently near the node. Although maize stalk lodging has been a subject of study for many years, relatively little is known about the process and progression of stalk failure. Of particular interest is the issue of failure initiation. An understanding of failure initiation could be beneficial talks that are less susceptible to failure. The purpose of this study was to characterize the tissue-level failure patterns of maize stalks. Various techniques were used to examine the failure region, including imaging (scanning electron microscope, X-ray computed tomography, photographs of the failure progression), experimentation (surface strain measurements, quantification of cross-sectional ovalization). We found that ovalization occurs prior to stalk failure and that ovalization is generally correlated with the onset of buckling. However, ovalization was predictive of failure. Tissue-level analysis revealed that buckling occurs at many different scales, including organ (specifically the stalk) level, tissue level, cellular level, and at the level of the cell wall. Based on our observations, we propose a new conceptual model for stalk failure that makes sense of the mixed data on this topic. This model states that the probability of tissue and buckling failure rise together in a highly correlated fashion and that when one failure mode occurs, it immediately initiates the corresponding mode. This information provides new insights into maize stalk failure and suggests that efforts to improve stalk strength will need to address both tissue strength and buckling resistance simultaneously. 

Cell migration is centrally involved in a myriad of physiological processes, including morphogenesis, wound healing, tissue repair, and metastatic growth. The bioenergetics that underlie migratory behavior are not fully understood, in part because of variations in cell culture media and utilization of experimental cell culture systems that do not model physiological connective extracellular fibrous networks. In this study, we evaluated the bioenergetics of C2C12 myoblast migration and force production on fibronectin-coated nanofiber scaffolds of controlled diameter and alignment, fabricated using a nonelectrospinning spinneret-based tunable engineered parameters (STEP) platform. The contribution of various metabolic pathways to cellular migration was determined using inhibitors of cellular respiration, ATP synthesis, glycolysis, or glucose uptake. Despite immediate effects on oxygen consumption, mitochondrial inhibition only modestly reduced cell migration velocity, whereas inhibitors of glycolysis and cellular glucose uptake led to striking decreases in migration. The migratory metabolic sensitivity was modifiable based on the substrates present in cell culture media. Cells cultured in galactose (instead of glucose) showed substantial migratory sensitivity to mitochondrial inhibition. We used nanonet force microscopy to determine the bioenergetic factors responsible for single-cell force production and observed that neither mitochondrial nor glycolytic inhibition altered single-cell force production. These data suggest that myoblast migration is heavily reliant on glycolysis in cells grown in conventional media. These studies have wide-ranging implications for the causes, consequences, and putative therapeutic treatments aimed at cellular migration.