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Understanding the role of SABP2-Interacting Proteins SIP432: a Premnaspirodiene Oxygenase Enzyme in Stress Signaling
No full textThis study focuses on the characterization of a SABP2-interacting protein (SIP)-432. SIP432 is a putative premnaspirodiene oxygenase-like P450 enzyme. Premnaspirodiene is a 15-carbon compound that can be converted into antimicrobial compounds by a hydroxylation reaction. The interaction of SIP432 with SABP2, a critical component of salicylic acid-mediated plant immunity, implies a role for SIP432 in plant stress signaling. This study uses the T-DNA knockout mutant of Arabidopsis thaliana SIP432 (homolog of NtSIP432) to help understand its role in abiotic and biotic stress responses. Plants were subjected to abiotic and biotic stress to understand their role in stress response pathways. Gene expression studies were also conducted to understand the changes in expression upon stress. This study will allow for the discovery of signaling in plant-stress interactions. Discovering the function of this protein could help uncover the signaling in plant stress pathways
State of the University Annual Report - 2024-2025
No full texthttps://dc.etsu.edu/president-annual-report/1010/thumbnail.jp
Wired for Addiction Decoding the Link Between Dopamine Dysregulation in Psychosis and Addiction Vulnerability
No full textStochastic Functional Data-Driven Models for Real-Time Battery Health Forecasting Under Dynamic Operating Conditions
No full textThis thesis provides an effective statistical model to predict the real-time state of lithium-ion batteries for reliable Battery Management Systems (BMS). It highlights battery data (voltage, current, temperature) as smooth functional curves. The principal method demonstrates diminishing trends to health outcomes like State of Health (SoH) and Remaining Useful Life (RUL) by employing Functional Principal Component Analysis (FPCA) and Bayesian Functional Linear Models (FLMs). The primary objective is to figure out how uncertain forecasts are. Simulations demonstrate that the highest accuracy (lowest MSE) is achieved through low noise levels along with large sample sizes. The final system provides a highly accurate and noise-resilient prognosis technique by integrating a multi-tier threshold monitoring system (e.g., 80\%, 50\% SoH) to translate forecasts into actionable warnings and predictive replacement schedules
Genetic Context Determines Mitochondrial and Longevity Outcomes of NAD+ Kinase Knockdown in Caenorhabditis elegans
No full textAging is characterized by progressive mitochondrial dysfunction and increased oxidative stress. NADPH is the essential reducing cofactor for antioxidant defense systems and lipid biosynthesis, but its levels decline with age in some tissues, partly due to age-related reduction of its precursor, NAD+. However, the relationship between NADPH depletion and mitochondrial impairment remains poorly understood. These studies describe how NADPH availability impacts mitochondrial function and longevity using Caenorhabditis elegans as a model organism. To induce NADPH depletion, NADP(H)-synthesizing enzymes including cytoplasmic nadk-1 (NADK), mitochondrial nadk-2 (NADK2), cytoplasmic pentose phosphate pathway (PPP) enzymes gspd-1 (G6PD) or T25B9.9 (PGD), mitochondrial idh-2 (IDH2), or mitochondrial men-1 (ME3) were knocked down across multiple genetic backgrounds. Mitochondrial oxygen consumption rates (OCRs), reactive oxygen species (ROS) production, ATP levels, lipid peroxidation, glutathione (GSH) levels, and lifespan were measured. Either cytoplasmic or mitochondrial NADPH depletion significantly decreased mitochondrial OCR and worm ATP levels but increased ROS levels and a lipid oxidative damage marker. The cellular response to cytoplasmic NADPH depletion was highly context-dependent. In wild-type worms, nadk-1 or gspd-1 knockdown increased oxidative damage but did not significantly affect lifespan. However, when cytoplasmic NADPH depletion was combined with a deficiency in a specific antioxidant pathway, the effects greatly differed. In trxr-1 mutants lacking cytoplasmic thioredoxin reductase-1, NADPH depletion mildly shortened lifespan, indicating the cytoplasmic thioredoxin system is essential for longevity when NADPH becomes limiting, whereas, in worms deficient for gsr-1, encoding cytoplasmic and mitochondrial glutathione reductase, or in cytoplasmic catalase ctl-1 mutants, NADP(H) depletion surprisingly decreased ROS levels and greatly extended lifespan, due to the activation of compensatory antioxidant stress responses. These findings reveal that the main H2O2 detoxification pathways have differential requirements for NADPH during aging. Cytoplasmic thioredoxin reductase appears critical for longevity under NADPH limitation, while deficiencies in glutathione reductase or cytoplasmic catalase allow for the induction of compensatory responses. This work demonstrates that genetic background profoundly influences whether NADP(H) depletion induces a pro-longevity antioxidant response, possibly providing insight into why antioxidant supplementation often fails to improve health. Understanding these context-dependent mechanisms may inform targeted therapeutic strategies to maintain mitochondrial health and extend healthspan during aging