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Jan 08 - 15, 2021

RPG Seminar Series (2021-01-08 & 2021-01-15)

Date: Friday, 8 January 2021

Venue: Seminar Room 2 & 3, G/F, Laboratory Block, Faculty of Medicine Building, 21 Sassoon Road, Pokfulam, Hong Kong [Mixed mode: Face-to-Face and Zoom]

Time: 5:00 p.m. - 6:00 p.m.

Zoom Link: https://hku.zoom.us/j/93151664316?pwd=Q0EyY241N1pyWnRKaER1NWVkcldYQT09

Meeting ID: 931 5166 4316

Password: 896548

Time: 5:00 p.m.
Speaker: Miss Xiaoqian HU (PhD candidate)
Primary Supervisor: Prof. Ying Shing CHAN
Presentation Title: Vestibular GABAergic inputs to head-direction network for navigation function
Abstract: 
Navigation is one of the most essential cognitive functions for survival, which requires accurate perception of direction through vestibular system. As the first station in head-direction network, the medial vestibular nucleus (MVN) is indispensable for integrating head movement signals. However, how GABAergic circuit in the MVN regulates vestibular output dynamics for spatial cognition remains unknown. We found that GABAergic interneurons in the MVN participate in sensory processing for navigation. Further dissection of these circuits by viral tracing revealed novel reciprocal long-range projecting inhibitory networks between MVN and relay stations in the ascending pathway. GABAergic inputs from MVN to the head-direction network were segregated between parvalbumin- (PV) and somatostain- (SST) neurons. Electrophysiology and combined chemo-/optogenetic manipulation will be used to further delineate their specific roles in navigation. Results hold promise for understanding the general mechanisms underlying cognition, as well as providing targets for novel therapeutic interventions for navigational deficits. 

Time: 5:30 p.m. 
Speaker: Mr. Aaron Wing Cheung KWOK (MPhil candidate)
Primary Supervisor: Dr. Joshua Wing Kei HO
Presentation Title: MQuad: Modelling of mitochondrial heteroplasmy for clonal substructure in single cell sequencing data
Abstract: 
Somatic mutations in the mitochondrial genomes (mtDNA) have been shown to have the capability to serve as natural cell barcodes for reconstructing clonal substructures and lineages in single cell sequencing data, such as scRNA-seq and scATAC-seq data. Not only are these data readily available and cost efficient, various highly multiplexed sequencing protocols have also been developed to further increase the resolution of subclonal structures in tumour tissues. However, we lack an effective computational method to model mtDNA heteroplasmy in noisy and sparse single-cell data. Here we introduce Mixture Modelling for Mitochondrial Mutations (MQuad), a computational tool that leverages a binomial mixture model to assess the heteroplasmy of mtDNA variants in a population of cells. Through a variety of simulated and experimental single cell sequencing data, we showed that using MQuad together with a tailored analysis suite, it can identify mitochondrial variants for robust inference of clonal substructure and evolutionary processes. Furthermore, we demonstrated its wide applicability in different protocols, particularly in complementing copy number variations to extract finer clonal resolution.


Date: Friday, 15 January 2021

Venue: Cheung Kung Hai Lecture Theatre 1, G/F, William M.W. Mong Block, Faculty of Medicine Building, 21 Sassoon Road, Pokfulam, Hong Kong [Mixed mode: Face-to-Face and Zoom]

Time: 5:00 p.m. - 6:00 p.m.

Zoom link: https://hku.zoom.us/j/93536327715?pwd=UkhHUWxzTmdvS0toY0J6MGRpbWthQT09

Meeting ID: 935 3632 7715

Password: 959594

Time: 5:00 p.m. 
Speaker: Miss Rachel Hiu Lam KWAN (PhD candidate)
Primary Supervisor: Dr. Chi Wai LEE
Presentation Title: ECM-induced formation of membrane infoldings regulate AChR trafficking during NMJ development
Abstract: At vertebrate neuromuscular junctions (NMJs), the junctional fold is a unique postsynaptic specialization formed by muscle membrane invagination during postnatal maturation. The mechanism underlying the formation of membrane specializations and their functional role in NMJ development remain elusive. Here, we first reported the requirement of extracellular matrix (ECM) proteins for membrane infolding formation at spontaneously formed aneural acetylcholine receptor (AChR) clusters in Xenopus muscle cultures. Super-resolution microscopy revealed a close resemblance between membrane infoldings at aneural AChR clusters and junctional folds at mature NMJs.  Lipid raft integrity is required for these structures, as demonstrated by impaired infolding formation and maintenance in membrane cholesterol-depleted or caveolin-3 knockdown muscles. Next, we identified the functional role of membrane infoldings as hotspots for AChR endocytosis upon synaptogenic stimulation. Collectively, this study demonstrates the involvement of caveolin-3 in ECM-induced membrane infoldings at aneural AChR clusters, which may regulate AChR trafficking and redistribution during synaptic formation.

Time: 5:30 p.m.
Speaker: Miss Yan Yi LAM (MPhil candidate)
Primary Supervisor: Dr. Kwok Ming YAO
Presentation Title: PDZD2 and Primary Open-Angle Glaucoma: Functional Study of the Silencer-Like Region in NT2 Neuronal Progenitor Cells
Abstract: Primary open-angle glaucoma (POAG) is a major cause of irreversible blindness worldwide. A single nucleotide polymorphism rs72759609, statistically significantly linked to POAG endophenotypes, was found within a highly conserved intronic region (~900 bp) of the PDZD2 locus. Here, deletion of this region was shown to upregulate PDZD2 expression in NT2 cells using western blot analysis, demonstrating its role as a silencer. Interestingly, Hedgehog (Hh) signalling was also found to be upregulated as reflected by an increase in expression of Gli1 but a decline in Gli3 level. Moreover, luciferase reporter assay revealed that the alternative allele (C) of rs72759609 is associated with lower gene expression when compared against with reference allele (T). Taken together, our data suggest that PDZD2/sPDZD2 positively modulates Hh signalling in NT2 cells and that decrease in PDZD2 expression via T-to-C mutation elevates the risk of developing POAG. Monitoring plasma sPDZD2 levels might be useful for POAG diagnosis.

 

ALL ARE WELCOME

Should you have any enquiries, please feel free to contact Miss Cecilia Chan at 3917 9493.