Date: Friday, 22 October 2021

Venue: Cheung Kung Hai Lecture Theatre 2, 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: Mr. Jifan YUAN (PhD candidate)
Primary Supervisor: Prof. Zhongjun ZHOU
Presentation Title: α-parvin is required for murine long bone development and regulates chondrocytes rotation
Abstract: Growth plate (GP) is a unique structure during long bone development. It provides cartilaginous mold for subsequent mineralization and bone formation. Integrin signaling mediates chondrocytes-ECM interaction and is required for chondrocytes differentiation, cytokinesis, rotation and proliferation. α-parvin is an integrin interacting protein that anchors the cytoskeleton to adhesion complex. Here, we show that loss of α-parvin in chondrocytes leads to dwarfism in mice and causes the long bones to become shorter but wider. Mutant chondrocytes show multiple defects like multinucleation and increased apoptosis which may partially explain the chondrodysplasia in mutant GP. By two-photon live imaging of fibula growth plates, we are able to visualize chondrocytes division and rotation in vivo. We prove that α-parvin is indispensable for chondrocytes post-division rearrangement or rotation, possibly due to altered cell-ECM and cell-cell adhesion.

5:30 p.m. 

Speaker: Mr. Shaobo YANG (PhD candidate)
Primary Supervisor: Dr. Bo GAO
Presentation Title: A potential PCP-independent function of Vangl2 on the endoplasmic reticulum
Abstract: The plasma membrane protein, Vangl2, is a core component of Planar Cell Polarity (PCP) signaling that governs a wide range of polarized cell behaviors. Despite the importance of Vangl2 in development and disease, its downstream signaling still remains poorly understood. Here, using BioID proximity labeling approach, we identified a Vangl2-interacting protein, VRK2, on the endoplasmic reticulum (ER) membrane, which is negatively regulated by Vangl2. Our preliminary data suggested that Vangl2 strongly binds with VRK2 on the ER membrane and recruits an ER localized E3 ligase, ZNRF4, to promote the ubiquitination and degradation of VRK2. Although the physiological function of such negative regulation is still under investigation, we found that loss of VRK2 leads to enlarged brain ventricles in mouse. Considering that VRK2 is a strong risk gene for schizophrenia, our findings suggest a potential novel function of Vangl2 in regulating neural development through a PCP-independent mechanism.

ALL ARE WELCOME

Should you have any enquiries, please feel free to contact Miss Cynthia Cheung at 3917 9748.