School of Biomedical Sciences cordially invites you to join the following Post-doctoral Fellow (PDF) Seminar:

Date: 13 May 2025 (Tuesday)
Time: 4:00 pm – 5:00 pm
Venue: Seminar Room 2, G/F, Laboratory Block, 21 Sassoon Road
Host: Dr. Haifeng Fu

Light refreshments will be served. Please register via the below link by 12 May 2025 (Monday):
Registration: https://hku.au1.qualtrics.com/jfe/form/SV_8IL60Ulfqz3mvJ4

Cryo-EM structural characterization of the functional amyloid Pipsqueak in the context of embryonic development
Dr. Pablo Adrian Guillen Poza (Post-doctoral Fellow)
[Supervisor: Professor Rubén Hervas Millan]

Prion-like proteins can adopt multiple conformational states and perform context-specific functions. Often associated with diseases like Alzheimer's and Parkinson's, these proteins also play crucial roles in physiological processes across different organisms. However, despite their prevalence, their functional significance remains largely unexplored. 

Combining imaging with biophysical analysis, we found that the transcription factor Pipsqueak exists as a monomer and a solid polymer in early Drosophila developing embryos. We isolated Pipsqueak from developing embryos and determined its activity and structure using cryo-electron microscopy. Both the monomer and polymer forms bind DNA, but only the polymer recruits with the polycomb protein, a key component of the PcG repressor complex. We postulate that the conformational change, stability, and self-renewing ability allow Pipsqueak amyloid to establish and maintain “memory” of transcriptional repression. By discerning structural disparities between functional and disease-associated amyloids, we aim to enhance our comprehension about amyloids and human diseases.

MMP14 deficiency in the chondrocyte-osteoblast lineage causes bone loss via depletion of skeletal progenitors and neutrophil accumulation
Dr. Anna Xiaodan Yu (Post-doctoral Fellow)
[Supervisor: Professor Kathryn Cheah]

Hypertrophic chondrocytes (HCs) in the growth plate contribute to endochondral bone growth by giving rise to osteoblasts in trabecular bone. Precise regulation of the HC differentiation program is critical for their proper lineage continuum. In this study, we found that the loss of MMP14 in HCs led to a decrease in trabecular bone in adult mice. Analysis by lineage tracing approach and H2B-GFP label-retaining experiment revealed a decrease in HC-derived osteoblasts and depletion of skeletal stem and progenitor cells (SSPC) in Mmp14cKO mice, suggesting that Mmp14 is necessary for maintaining chondrocyte-osteoblast lineage continuum and SSPC. The activation of neutrophils was detected in the hypertrophic zone-trabecular region and bone marrow of Mmp14cKO mice. Cell-cell interactions between immature neutrophils and osteogenic cells were identified. Overall, this study provides insights into the role of Mmp14 in maintaining bone homeostasis and highlights the importance of HC-derived cells in bone formation and immune regulation.

All are welcome.