Date:18 April 2024 (Thursday)
Time: 5:00 pm – 6:00 pm
Venue: Cheung Kung Hai Lecture Theatre 1, G/F, William M.W. Mong Block, 21 Sassoon Road

5:00 p.m.

Presenter: Kan Shing Kevin NG (PhD candidate)
Primary Supervisor: Prof. Rubén HERVAS MILLAN
Presentation Title: The structural basis of Pipsqueak amyloid assembly during embryonic development for functional insight
Abstract: Prion-like proteins can adopt distinct conformations, including a self-perpetuating aggregated state. While typically associated with disease, these assemblies also orchestrate various biological processes across different organisms. Previously, we performed a proteome screen of Drosophila melanogaster and identified Pipsqueak (psq) as a potential prion-like protein. Psq is a transcription regulator known for determining cell fate during Drosophila embryonic development. To this end, psq recruits polycomb group (Pc-G) repressor complexes to specific DNA elements, known as polycomb response elements (PREs), to assist them to exert their repressive function on diverse developmental genes.

We found that the longest psq isoform (psqL) adopts two conformational states in vivo: a monomeric state and a self-perpetuating aggregated state. The aggregated psqL, resembling an amyloid, assembles after nuclear division in the early developing embryo, effectively recruits the Pc-G repressor complex, and disassembles as cell division ensues. Thus, we propose that psqL conversion from a monomer to a self-perpetuating amyloid state in developing embryos epigenetically perpetuates the repressive state of Pc-G loci targets.

5:30 p.m.

Presenter: Jia Ying NG (PhD candidate)
Primary Supervisor: Prof. Martin CHEUNG
Presentation Title: Elucidating the role of DOCK7 in melanoma development
Abstract: Melanoma is the most malignant form of skin cancer with high lethality. Analysis of the TCGA database showed higher expression levels of DOCK7, a guanine exchange factor for RHO-GTPases, in specimens from melanoma patients than in normal tissue samples. In vitro and in vivo functional studies showed that DOCK7 plays a critical role in promoting melanoma growth, tumorigenicity, and metastasis, independent of its GEF activity. To investigate the mechanisms by which DOCK7 regulates tumorigenesis in melanoma, mass-spectrometry analysis revealed that HIF1a, as an interacting factor of DOCK7, is highly expressed in melanoma cells as compared to melanocytes under normoxia conditions. DOCK7 knockdown led to a marked reduction in both mRNA and protein levels of HIF1a. Overexpression of HIF1a promoted melanoma proliferation. Mechanistically, DOCK7 regulates the transcription of HIF1a via the AKT pathway. Future studies will focus on elucidating the interplay between DOCK7 and HIF1a in promoting tumorigenesis in melanoma.

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