Amy
Fulton
Recent years have featured a stark rise in global temperatures, and the coming years only point to the continuation of this trend. This has impacted the migration and habitat patterns of many animal species to maintain their optimal habitat climate. However, stationary plants bear the risk of reduced growth in these hotter temperatures. One possible solution is genetically modifying plants to grow better in temperature-stress conditions, and this involves the manipulation of genes involved in biomolecular condensate formation. Biomolecular condensates are membrane-less organelles composed of proteins and RNA, which control many cellular processes on a biochemical level including the responses to environmental changes like temperature. Previous studies have found that the Auxin Response Factors, (ARF7 and ARF19) form condensates that regulate auxin signaling in roots, a phytohormone critical for overall plant growth. Further analysis of gene structure has shown that the Intrinsically Disordered Region (IDR) in ARF19 is necessary for the formation of condensate. Research within the Strader Lab currently focuses on swapping the ARF19-IDR region with two diPerent polypeptides: Resilin-like polypeptides (RLPs) and Elastin-like polypeptides (ELPs). These artificial peptide polymers have been previously shown to phase separate at diPerent temperatures. In particular, RLP undergoes phase separation (condensate formation) at low temperatures, and ELP undergoes phase separation at high temperatures. The goal of this research is to analyze the ePect of these peptide swaps on temperature regulation in Arabidopsis thaliana and create a functional temperature-sensing mechanism in the plant. Preliminary results through protoplast transfection show that some of these RLPs and ELPs respond to changes in temperature through phase separation. Further analysis in transgenic lines expressing the ARF19 with these polypeptide swaps will assist in generating thermosensor plants. Successful temperature regulation of these thermosensor plants would suggest a method of vegetation survival despite the growing stressors of the global climate. Activity of Intracellular Mediators in Post-TBI Epilepsy and Inflammatory Response
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Amy Fulton
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Inflammatory response following TBI is implicated in post-traumatic epileptogenesis, although the exact pathway and mechanism remains unclear. The lifetime burden of both TBI and epilepsy are high, and especially when they are concurrent. Our study probed the expression of several proteins implicated in a proposed neural response pathway in groups of mice subjected to TBI, inflammation-causing agents, and both, across various time points. Ten mice were divided into four groups: sham (untreated), LPS-treated, TBI-injured, and LPS + TBI. Mice were first treated with LPS, if applicable, to induce inflammation. Mice were then injured with TBI at a 3mm displacement. Brain was fixed at time points of 3, 6, 9, and 24 hrs. Protein isolation and concentration assays were completed using these experimental animals at each time point. All results were compared to findings in control (sham/untreated) animals to account for the neurological ePects of surgical anesthesia. Findings included high BDNF expression at 3 and 9 hours in LPS-treated groups, as well as slightly elevated levels at 9 hours in the TBI-only group. IL1-Ra expression lingered at high levels for much longer in TBI + LPS mice than in TBI-only or LPS-only mice. AIF1 peaked at 6 hours in both TBI groups, but not in the LPS-only group. IKBa expression was relatively similar across groups, but all treated groups (TBI, LPS, and TBI + LPS) showed very high levels of pIKBa at 6 hours compared to controls. NFKB showed increased expression at 24 hours in both LPS-treated groups, and pNFKB spiked at 6 hours in all groups, especially LPS and LPS + TBI. LRP showed relatively consistent expression across all groups and time points. Expression of most all proteins was highest at 6 hours, except BDNF which peaked at 9 hours. These results provide potential insight into the regulation of inflammatory response following TBI and inflammation, including potential overlap and divergence in pathways.
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Duke University / 2024
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Amy Fulton