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Nov 24, 2021

PDF Seminar (2021-11-24)

Date: Wednesday, 24 November 2021

Venue: Cheung Kung Hai Lecture Theatre 3, G/F, William M.W. Mong Block, Faculty of Medicine Building, 21 Sassoon Road, Pokfulam, Hong Kong

Time: 5:00 p.m. - 6:00 p.m.

5:00 p.m.

Speaker: Dr. Sophia Ka Yan MA (Post-doctoral Fellow)
Primary Supervisor: Prof. Danny CHAN
Presentation Title: Planarian collagens regulate pluripotency and progenitor cell populations during homeostasis and regeneration
Abstract: Planarians are flatworms that possess incredible regenerative abilities due to a large heterogeneous population of pluripotent stem cells. While signaling pathways that regulate the planarian stem cell population has been extensively studied, the role of the extracellular matrix in the stem cell niche is less understood. Type IV collagen was identified from a mass RNAi screening of ECM genes, as a regulator of proliferation and differentiation of the stem cell population. Knockdown of planarian col4-1 leads to hyperproliferation of stem cells, however these stem cells do not differentiate to mature cell types during homeostasis and regenerative processes. In contrast, knockdown of 3 out of 11 fibrillar collagen genes lead to a decrease in stem cell proliferation. Furthermore β-Aminopropionitrile (BAPN) inhibition of lysyl-oxidase, a collagen crosslinking enzyme, negatively impacts the rate of planarian regeneration. While the ECM plays a major role in the regulation of biochemical signaling, it is also involved in mechanical signals that can alter cell behavior. RNAi screening of genes involved in mechanotransduction revealed a role of Piezo ion channel in regulating the anterior-posterior axis during regeneration. Understanding how the planarian ECM regulates both biochemical and mechanical signals will provide insights into how the regenerative process is tightly regulated through a combination of signals.

5:30 p.m. 

Speaker: Dr. Yan XUE (Post-doctoral Fellow)
Primary Supervisor: Dr. Joshua Wing Kei HO
Presentation Title: Somatic mitochondrial DNA mutations enable clonal tracking in nasopharyngeal carcinoma at single cell resolution
Abstract: Reconstruction of clonal dynamics in cancer is critical to understand tumor progression and implement personalized therapies. Somatic mitochondrial DNA (mtDNA) mutations have recently been recognized as natural genetic barcodes to infer clonal relationships in single cell RNA sequencing data. However, the low sequencing depth and uneven read coverage of current standard droplet-based scRNA-seq technology, as well as lack of effective computational mitochondrial variant calling method constraint the application of mtDNA mutation in clonal dynamic inference. To overcome these challenges, we adapted and tested a recently developed protocol called MAESTER (Mitochondrial Alteration Enrichment from Single-cell Transcriptomes to Establish Relatedness) to enrich all 15 mitochondrial transcripts from full length cDNA barcoded scRNA-seq libraries generated by the 10X Genomics platform. We tested this method on five human clinical samples from nasopharyngeal carcinoma (NPC) patients. Preliminary data suggest that MAESTER can generate reads with higher and more even coverage across all mitochondrial transcripts, hence significantly enhancing the ability to detect clone-specific somatic mtDNA mutations at the single cell level.  This new experimental method will be used in conjunction with our newly developed bioinformatics tool MQuad (Mixture Modelling of Mitochondrial Mutations) to chart the clonal landscape in NPC.



Should you have any enquiries, please feel free to contact Miss River Wong at 3917 9216.