Apoptosis is a growth regulating process in mammals that may be conserved across eukaryotes. While some apoptotic markers, DNA fragmentation and release of reactive oxygen species (ROS), appear in yeast, it is unclear whether they indicate stress response or apoptosis. We can use live cell microscopy (LCM) to quantify ROS in yeast grown in stresses. Once ROS appear, cells never bud again, indicating an apoptotic pathway. Furthermore, mammalian SRPK2 may be cleaved; the N-terminus translocates to the nucleus and may induce an apoptotic pathway. Yeast encode the SR protein kinase, Sky1, whose deletion reduces the presence of apoptotic markers compared to wild-type. Under stress, WT cells grow worse than sky1? and better than sky1-overexpression constructs. LCM data comparing ROS are consistent. We investigate Sky1 cleavage using N- and C-terminal fluorescent tags. Determining that these results represent an apoptotic pathway opens the door to using yeast to further probe apoptotic mechanisms._x000D_
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Easel 7: Optic nerve regeneration in Xenopus laevis: intact myelin removal and gene expression_x000D_
Tara Loughery, Matt Bryson, Weldon Furr_x000D_
Amphibians are able to regenerate their optic nerve into adulthood, whereas mammals lose this ability before birth. Here, we explore the role of myelin in optic nerve recovery and whether myelin debris hinders regeneration. Specifically, we crush optic nerves and collect them at various time points up to 210 days post-surgery (dps). Using a line of frogs expressing GFP in retinal ganglion cell axons, we establish a timeline of axonal recovery showing full recovery does not occur until day 210. Preliminary data shows intact myelin is absent in nerve segments distal and proximal to the injury by 7 and 11dps, respectively and was not detected by 210dps. Here we also explore protein expression patterns of ?- synuclein and Uchl1, two factors thought to play a role in optic nerve regeneration. These data will help fill a knowledge gap in understanding the basic mechanisms underlying nerve regrowth and regeneration._x000D_
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Easel 8: Friend or Foe: Manipulating Nestmate Recognition and Olfaction in Carpenter Ants_x000D_
Chris Myers_x000D_
Discriminating between friends and foes is imperative for the survival of social insects like ants, termites, and bees. When friends (nestmates) are together, they often participate in social grooming, group foraging, and food-sharing. When enemies (non-nestmates) are together, they will display context-specific aggression behaviors to protect their colonies. The ant species Camponotus pennsylvanicus uses unique combinations of cuticular hydrocarbon (CHC) cues to distinguish between colonies. However, it is debated whether this detection relies on the recognition of nestmates via familiar CHC profiles, or non-nestmates via unfamiliar ones. To address this question, we can manipulate odorant receptor activation as well as individual CHC profiles and observe the resulting changes in social recognition behavior. Using these strategies to modify the aggression behaviors, we hope to provide support toward one model of CHC-based nestmate discrimination._x000D_
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Easel 9: Constant access to snacks from weaning to adulthood in female rats induce early signs of obesity even before weight gain._x000D_
Lauren Arcinas, Gunnar Bowman, Leslie dela Cruz, Mariam Samuel_x000D_
We developed a female snacking rat model to investigate the mechanisms leading to childhood obesity. We hypothesized that constant access to snacks after weaning causes an early onset of metabolic syndrome. Rats received chow only, healthy snacks, or unhealthy snacks (n=8/group), and all received chow and water. Food intake, snack intake, and body weight were monitored daily. Both snacking groups weighed significantly more than chow-fed rats and had larger abdominal fat pads despite eating fewer calories. Leptin challenges showed that all pubertal rats were resistant to leptin’s ability to reduce food intake, and that snacking rats remained resistant to leptin as adults. A glucose tolerance test determined that snacking rats developed insulin resistance as adults. Thus, constant access to snacks induced early onset of metabolic syndrome. In addition, young rats, and probably humans, are vulnerable to snacks from weaning due to inherent leptin resistance that is sustained into adulthood.
