Title: Studying the evolution of peri-phallic novelty in Drosophila
Abstract:
In evolutionary developmental biology, the evolution of novel morphology is a key mechanism in the emergence of diversity and an important step toward specialization; as such, it is a critical point of study. The posterior lobe, an outgrowth of the lateral plate, is hypothesized to have emerged recently in the last common ancestor of Drosophila melanogaster and Drosophila yakuba. Since its emergence, the posterior lobe has rapidly diversified in various species, which makes it an excellent model for studying the emergence and diversity of novel traits.
Drosophila auraria, a more distantly related species, exhibits a "lobe-like" structure. At the same time, other common relatives that more recently diverged from D. melanogaster do not exhibit any lobe-like phenotype. In this presentation, I will show preliminary data indicating that the D. auraria pseudo-lobe does not share conserved gene expression but does share development patterns with the D. melanogaster posterior lobe, potentially pointing towards a convergent origin. More specifically, I will utilize methods such as HCR and ECAD antibody staining to visualize gene expression patterns and tissue development, respectively.
I also aim to characterize other closely related "non-lobed" species using the aforementioned techniques to identify potential lobe-like structures and genes essential for lobe formation. The results of these analyses should provide critical insights into the evolution of novel morphologies.
Title: Investigating transcription dynamics in murine embryonic stem cells through rapid depletion of nucleosome remodelers
Abstract:
Nucleosome remodelers govern DNA-based processes such as transcription and replication by altering the position and composition of nucleosomes. Past studies have demonstrated that select remodelers are required for driving appropriate mRNA expression; however, the role of many remodelers in regulating mRNA expression and most remodelers in regulating the expression of non-coding RNA (ncRNA) remains elusive. A comprehensive study from the Hainer lab addressed this gap by independently knocking down each nucleosome remodeler ATPase in mouse embryonic stem (mES) cells to delineate mRNA and ncRNA transcription changes 48 hours post-knockdown. However, the extended knockdown period could introduce indirect effects on RNA profiles; therefore, I aim to rapidly deplete a subset of nucleosome remodelers to determine direct roles of remodelers.
The same study from our lab uncovered acute upregulation of specific nucleosome remodelers upon knocking down other remodelers, suggesting potential compensation mechanisms where an alternative remodeler is upregulated due to remodeler loss. For example, upon depletion of Chd4, we observed transcriptional upregulation of Chd3 and Chd5. Chd3/4/5 are mutually exclusive ATPase subunits of the NuRD nucleosome remodeling complex. While Chd3 and Chd5 are not highly expressed in mES cells, I hypothesize that upon CHD4 loss, CHD3 and CHD5 are upregulated to be incorporated in the NuRD complex to compensate for CHD4 loss. My preliminary data demonstrate that Chd4 knockdown results in increased Chd3 and Chd5 mRNA and protein levels. Therefore, I aim to further examine the Chd3/Chd5 expression profile through rapid depletion of Chd4 and investigate the compensatory mechanism among these remodelers.
Rebeiz and Hainer Lab
Friday, September 6th, 2024
12:00PM
Langley A219B