Decreasing Hunchback and Bicoid Levels in Pair1 Neurons Alters the Pair1 Circuit in Drosophila

Presenter: Amanda Linskens – Biochemistry

Faculty Mentor(s): Kristen Lee, Chris Doe

Session: (In-Person) Poster Presentation

Transcription factors (TFs) are essential for cell specification across multiple species, including humans. During Drosophila melanogaster development, neuroblasts produce neuronal progeny that acquires identity based on the temporal TF (tTF) present during birth. tTFs activate specific Homeodomain TFs (HDTFs), which are also important for determining neuronal identity. Thus, the cascade of tTFs in neuroblasts creates the diversity necessary for forming precise neural circuits. Although prior research shows that TFs generate variety, few studies have examined how these TFs influence circuit establishment. My study focuses on the Pair1 neurons, which initiate pausing in larvae through neural circuits. Prior research in our laboratory showed that the Pair1s derive from the tTF Hunchback (Hb), which activates the HDTF Bicoid (Bcd). Therefore, I hypothesized that manipulating Hb’s and Bcd’s expressions in Pair1 would alter the Pair1 circuit. To investigate this,

I expressed the green fluorescent protein (GFP) in the Pair1s and knocked down Hb and Bcd levels individually to assay circuit morphology and behavior. I found that decreasing Hb resulted in more Pair1 axonal connections, affecting behavior. Interestingly, I saw similar results when Bcd was knocked down in Pair1, but the phenotypes are weaker than those experienced with decreased Hb levels. These results suggest that tTF activation of HDTFs is vital for circuit establishment in the central nervous system.

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