Novel roles for ecdysone receptor in the Drosophila germline

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dc.access.optionRestricted Campus Access Only
dc.contributor.advisorAbles, Elizabeth Tweedie
dc.contributor.authorPhipps, Daniel Noah
dc.contributor.committeeMemberHorn, Patrick J
dc.contributor.committeeMemberStellwag, Edmund J
dc.contributor.departmentBiology
dc.date.accessioned2023-02-07T18:37:19Z
dc.date.available2024-07-01T08:01:59Z
dc.date.created2022-07
dc.date.issued2022-07-01
dc.date.submittedJuly 2022
dc.date.updated2023-01-31T21:26:54Z
dc.degree.departmentBiology
dc.degree.disciplineMS-Biology
dc.degree.grantorEast Carolina University
dc.degree.levelMasters
dc.degree.nameM.S.
dc.description.abstractOogenesis, the process by which a viable egg is produced, demands carefully coordinated communication between somatic and germ cell populations, relying on both local and systemic factors such as steroid hormones for signaling. In Drosophila, the steroid hormone ecdysone is crucial for a variety of physiological processes throughout development and adulthood, including oogenesis. Ecdysone signaling largely relies on the nuclear receptor Ecdysone Receptor (EcR) to receive the hormone as a ligand, resulting in transcriptional activation and regulation of downstream targets. The relative contribution of EcR in germ cells versus somatic cells for proper oogenesis, however, is unknown. Previous analyses of EcR function in oogenesis relied on manipulation of somatic cell types or global mutations, leaving the role for EcR in the germline rather speculative. A lack of germline-compatible tools to study EcR has been a key contributor to this knowledge gap. To address this, we generated three germline-enhanced UAS-RNAi lines against EcR that effectively reduce EcR mRNA levels in germ cells. Consistent with the phenotype of EcR global mutants, depletion of EcR in germline mosaics and ubiquitously in all germ cells depletes the number of germline stem cells over time. Intriguingly, we also find that knockdown of EcR in germ cells results in phenotypes not previously linked to ecdysone signaling. We demonstrate that depletion of EcR in germ cells disrupts encapsulation of 16-cell cysts as they move posteriorly to form egg chambers. This suggests that EcR is required specifically in germ cells for them to actively contribute to their own encapsulation and posits that EcR may have unique transcriptional targets in germ cells at this stage of oogenesis. These tools will be highly useful in future studies to understand how ecdysone signaling impacts the relationship between the germline and soma during oogenesis.
dc.embargo.lift2024-07-01
dc.format.mimetypeapplication/pdf
dc.identifier.urihttp://hdl.handle.net/10342/12197
dc.language.isoen
dc.publisherEast Carolina University
dc.subjectoogenesis
dc.subjectecdysone
dc.subjectDrosophila
dc.titleNovel roles for ecdysone receptor in the Drosophila germline
dc.typeMaster's Thesis
dc.type.materialtext

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