Understanding the relationship between PLA2G6 in somaticcells and the female germline
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Abstract
Improved healthcare and lifestyle efficiencies, such as sanitation and nutrition, has led to a longer life expectancy worldwide and thus an increase in age-related illnesses, such as Parkinson’s disease (PD). PLA2G6 has been identified as a gene of interest in the development of both inherited and sporadic PD 1,2. My mentor’s lab has previously found3 that a full somatic knockdown of the Drosophila homolog for PLA2G6, iPLA2-VIA, led to locomotor decline in Drosophila and further, that tissue-specific knockdown of iPLA2-VIA in neurons and muscles led to locomotor defects, similar to the locomotor decline seen in human PD patients. iPLA2-VIA was also found in the male and female germline, affecting female fertility. A full somatic knockdown of iPLA2-VIA also resulted in reduced female fertility and abnormal mitochondrial aggregation in the female germline. This novel relationship between somatic knockdown of iPLA2-VIA and reduced female fertility was the impetus leading to my research. Similar to the identification of tissue locus effects on locomotor abilities, I set out to identify the specific tissue types that contribute to the female fertility decline and mitochondrial aggregation. We found that the knockdown of iPLA2-VIA in neuronal tissue leads to reduced female germline mitochondrial integrity, fertility, and increased apoptosis. Expression of iPLA2-VIA in muscle tissue may also be found to affect germline health while expression in follicle cells and fat bodies did not reveal a relationship with female germline health. Furthermore, starvation was ruled out as a potential confounding variable in reduced fertility, in mitochondrial damage, and increases in apoptosis. Lastly, fat bodies were shown to not have an effect on Drosophila locomotor abilities. Studying the root, forms, and pathophysiology of PD and related conditions can aid in identifying potential medicinal routes for treatment.