The circadian fluctuation of melatonin in \u3cem\u3eStenostomum virginianum\u3cem\u3e

Much is known about melatonin and its role in the circadian regulation of vertebrate organisms. However, melatonin has not been studied extensively in more primitive bilaterians. The aim of this study was to analyze the relationship between melatonin and the circadian rhythm in the organism Stenostomum virginianum. Melatonin assay methods from previous research in the field were optimized for smaller tissue sampling of microscopic metazoans. The optimized assay methodology was then used to identify melatonin in Stenostomum virginianum using high performance liquid chromatography (HPLC). Identification of photoreceptors was used to correlate the presence of melatonin to the circadian rhythm. PAX-6 was chosen for study because it is considered the master eye regulatory gene. Immunohistochemistry and confocal microscopy confirmed the presence of PAX-6 in the anterior region of S. virginianum. The next step in this project is the examination of melatonin concentration at various time points and the comparison of the fluctuation pattern to the S. virginianum sleep and reproduction cycles. Following this comparison, the next logical step is the analysis of melatonin biosynthetic enzymes. This project builds on the work of Dan Stanton and Julian P. Smith, PhD

Basal Mitophagy Occurs Independently of PINK1 in Mouse Tissues of High Metabolic Demand

Dysregulated mitophagy has been linked to Parkinson’s disease (PD) due to the role of PTEN-induced kinase 1 (PINK1) in mediating depolarization-induced mitophagy in vitro. Elegant mouse reporters have revealed the pervasive nature of basal mitophagy in vivo, yet the role of PINK1 and tissue metabolic context remains unknown. Using mito-QC, we investigated the contribution of PINK1 to mitophagy in metabolically active tissues. We observed a high degree of mitophagy in neural cells, including PDrelevant mesencephalic dopaminergic neurons and microglia. In all tissues apart from pancreatic islets, loss of Pink1 did not influence basal mitophagy, despite disrupting depolarization-induced Parkin activation. Our findings provide the first in vivo evidence that PINK1 is detectable at basal levels and that basal mammalian mitophagy occurs independently of PINK1. This suggests multiple, yet-tobe- discovered pathways orchestrating mammalian mitochondrial integrity in a context-dependent fashion, and this has profound implications for our molecular understanding of vertebrate mitophagy