Modeling the Effect of Post-Dispersal Seed Predation on Tropical Tree Species in Panama

Palm trees provide a unique opportunity to study what conditions optimize the probability that a seed will grow successfully. The seeds of palm trees, endocarps, are large and easy to locate. When they don\u27t grow, predators leave marks on them that tell the story of their fate. The focus of my experiment is to determine how the current distribution pattern of parent palm trees in Panama Palm trees affects the the future distribution of seedlings. I have programmed a versatile model that takes the assumption that bruchid beetles are the sole predators acting on the seeds, and that these fall from the trees in an inverse logarithmic density pattern. The beetles are programmed to move to a random seed within an arbitrary distance of their start point. If no seeds are near enough to them, then they starve. I hypothesize that the beetles will decrease clumping within five generations.https://digitalcommons.usu.edu/fsrs2018/1010/thumbnail.jp

Emergent Seedling Spatial Patterns Following Insect Seed Predation in a Simulated Population

Tropical vertebrate species have faced increasing pressures from hunters, causing many to become locally extinct. I used an agent-based model (NEDD) to investigate the influence of dispersal and insect seed predation on seedling survival. Statistical dispersal kernels were used to simulate the dispersal of seeds. The NEDD model generates survival and spatial data from parameter sets, which were chosen based on a Latin-Hypercube experimental design. Spatial point analysis was performed on the output data to identify trends in spatial clustering patterns as the parameter space was changed. The results of this investigation suggest that there is a positive association between the proportion of seeds that are distributed at a frugivore site and the successful recruitment of seeds. Increasing frequency of frugivore sites was shown to have a negative impact on seedling recruitment. Understanding the role of tropical vertebrates in mediating seed dispersal and survival may inform management decisions in the near future

Tracing Brain Structures of Alkali Bees to Investigate Endocrine and Social Effects on Neural Plasticity

For highly social bee species, juvenile hormone (JH) and social cues are linked to increased expression of class-based social features. However, little data has been collected on the relationship between these variables and homologous features in non-social bees. To fill this gap in data, we studied the neuroanatomical response of Nomia melanderi, a non-social bee species, to endocrine and social treatments. Since N. melanderi is a non-social bee with pre-adaptations to sociality, such as brood care and aggregative nesting habits, its responses to hormone treatment and social cues can be used to model how neural plasticity in non-social ancestors of highly social bee species may have played a role in social evolution. Specifically, we measured volumetric difference in mushroom body structures, which are known to function in social cognition in social bees, in response to our treatments. Brains from the six treatment groups were dissected and imaged using confocal microscopy techniques. By scaling the actual distance in an image to its pixel density, reliable measurements of volume are produced from evenly spaced cross-sections of N. melanderi brain. Since data collection for the current phase of the project is still underway, it’s premature to make any conclusion about how JH and social cues influence neural plasticity in N. melanderi. However, the results of our experiment are likely to provide unique insights into the evolution of sociality in bee species generally.

Glucocorticoid signaling enhances expression of glucose-sensing molecules in immature pancreatic beta-like cells derived from murine embryonic stem cells in vitro

Pluripotent stem cells may serve as an alternative source of beta-like cells for replacement therapy of type 1 diabetes; however, the beta-like cells generated in many differentiation protocols are immature. The maturation of endogenous beta cells involves an increase in insulin expression starting in late gestation and a gradual acquisition of the abilities to sense glucose and secrete insulin by week 2 after birth in mice; however, what molecules regulate these maturation processes are incompletely known. Here, we aim to identify small molecules that affect immature beta cells. A cell-based assay, employing pancreatic beta-like cells derived from murine embryonic stem (ES) cells harboring a transgene containing an Insulin 1-promoter driven enhanced green fluorescent protein reporter, was used to screen a compound library (NIH Clinical Collection-003). Cortisone, a glucocorticoid, was among five positive hit compounds. Quantitative RT-PCR analysis revealed that glucocorticoids enhance the gene expression of not only insulin 1 but also glucose transporter-2 (Glut2; Slc2a2) and glucokinase (Gck), two molecules important for glucose sensing. Mifepristone, a pharmacological inhibitor of glucocorticoid receptor (GR) signaling, reduced the effects of glucocorticoids on Glut2 and Gck expression. The effects of glucocorticoids on ES-derived cells were further validated in immature primary islets. Isolated islets from 1-week-old mice had an increased Glut2 and Gck expression in response to a 4-day treatment of exogenous hydrocortisone in vitro. Gene deletion of GR in beta cells using rat insulin 2 promoter-driven Cre crossed with GRflox/flox mice resulted in a reduced gene expression of Glut2, but not Gck, and an abrogation of insulin secretion when islets were incubated in 0.5 mM D-glucose and stimulated by 17 mM D-glucose in vitro. These results demonstrate that glucocorticoids positively regulate glucose sensors in immature murine beta-like cells

Playing the Public Lands Game- HONR 3020: Engaging Utah\u27s Public Lands

How to get involved with public land issues and learn what\u27s at stake. Join us as students present a guide that teaches how to locate, navigate, and participate in the various government and public processes for engaging in public lands debates

Glucocorticoid signaling enhances expression of glucose-sensing molecules in immature pancreatic beta-like cells derived from murine embryonic stem cells in vitro

Pluripotent stem cells may serve as an alternative source of beta-like cells for replacement therapy of type 1 diabetes; however, the beta-like cells generated in many differentiation protocols are immature. The maturation of endogenous beta cells involves an increase in insulin expression starting in late gestation and a gradual acquisition of the abilities to sense glucose and secrete insulin by week 2 after birth in mice; however, what molecules regulate these maturation processes are incompletely known. Here, we aim to identify small molecules that affect immature beta cells. A cell-based assay, employing pancreatic beta-like cells derived from murine embryonic stem (ES) cells harboring a transgene containing an Insulin 1-promoter driven enhanced green fluorescent protein reporter, was used to screen a compound library (NIH Clinical Collection-003). Cortisone, a glucocorticoid, was among five positive hit compounds. Quantitative RT-PCR analysis revealed that glucocorticoids enhance the gene expression of not only insulin 1 but also glucose transporter-2 (Glut2; Slc2a2) and glucokinase (Gck), two molecules important for glucose sensing. Mifepristone, a pharmacological inhibitor of glucocorticoid receptor (GR) signaling, reduced the effects of glucocorticoids on Glut2 and Gck expression. The effects of glucocorticoids on ES-derived cells were further validated in immature primary islets. Isolated islets from 1-week-old mice had an increased Glut2 and Gck expression in response to a 4-day treatment of exogenous hydrocortisone in vitro. Gene deletion of GR in beta cells using rat insulin 2 promoter-driven Cre crossed with GRflox/flox mice resulted in a reduced gene expression of Glut2, but not Gck, and an abrogation of insulin secretion when islets were incubated in 0.5 mM D-glucose and stimulated by 17 mM D-glucose in vitro. These results demonstrate that glucocorticoids positively regulate glucose sensors in immature murine beta-like cells