Date: Friday, 27 May 2022

Time: 5:00 p.m. - 6:00 p.m.

Venue: Cheung Kung Hai Lecture Theatre 1, G/F, William M.W. Mong Block, 21 Sassoon Road, Pokfulam, Hong Kong

5:00 p.m.

Presenter: Miss Zihan XU, PhD candidate
Primary Supervisor: Dr. Martin CHEUNG
Presentation Title: Elucidating the role of Deleted in Liver Cancer 1 (DLC1) in human neural crest development
Abstract: Neural crest cells (NCCs) are a population of multipotent embryonic stem-like cells that arise at the neural plate border along the cranial/caudal axis. A gene regulatory network orchestrates the formation, migratory properties, and lineage differentiation of NCCs. Our previous studies in chick embryos showed that an appropriate expression level of Deleted in Liver Cancer 1 (DLC1), a RhoGTPase-activating protein, is required for cranial NC formation. To further extrapolate the findings from chick to human, we used human induced pluripotent stem cells (hiPSCs) to differentiate into NCCs via induction of neural plate border (NPB)-like cells to elucidate the role of DLC1 in NC development. Our results reveal that human DLC1 isoform 2 (DLC1-i2) expression was initiated in NPB-like cells and maintained in early NCCs. Subsequently, DLC1 isoform 1 (DLC1-i1) expression was initiated in early NCCs and maintained at a considerable level with NC markers expression. shRNA-mediated knockdown of DLC1 in hiPSCs led to a decreased expression of NC markers compared to scramble control. In contrast, DLC1-i1 overexpression (OE) promoted migratory NC-like cell formation at the expense of NPB-like cells and early NCCs. DLC1-i2 OE retained cells at the NPB state as evidenced by increased expression of NPB markers and reduced expression of NCC markers. Altogether, these results suggest that human DLC1 has a conserved expression and function with its chick counterpart during early NC development, and its isoform switching is crucial for the transition from NPB-like cells to a committed NCC fate. Importantly, we found the addition of DLC1 isoform together with other transcription factors could further enhance reprogramming efficiency from somatic cells into induced NC-like cells with cranial character, paving the way for the modeling of craniofacial disorders and therapeutic development.

5:30 p.m.

Presenter: Miss Sherry Sin Hang YEUNG, PhD candidate
Primary Supervisor: Dr. Raymond CHANG
Presentation Title: Investigating the borders between peripheral and neuroimmune crosstalk in a zebrafish model of neurodegenerative tauopathy
Abstract: Traditionally understood to be an immune-privileged organ, immunity within the brain and the periphery has been studied independently. Little appreciation is given to the immune crosstalk between peripheral organs and the CNS, and to a lesser extent its putative effects on regulating neurodegeneration. Here, we demonstrate through a zebrafish model of fin amputation that macrophage/monocytes can facilitate immune crosstalk between the periphery and the brain, which further exacerbates neuropathological hallmarks in a zebrafish model of neurodegenerative tauopathy. We propose that this peripheral-neuroimmune crosstalk is facilitated by circulatory mechanisms independent of blood vasculature. 

ALL ARE WELCOME

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