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

Date: 25 February 2025 (Tuesday)
Time: 4:00 pm – 5:00 pm
Venue: Lecture Theatre 1, G/F, William M.W. Mong Block, 21 Sassoon Road
Host: Dr. Haifeng Fu

Light refreshments will be served. Please register via the below link by 24 February 2025 (Monday):
Registration: https://hku.au1.qualtrics.com/jfe/form/SV_0PR7FMBKn3uZdki

Multipotent neural stem cells originating from neuroepithelium exist outside of the mouse central nervous system
Dr. Dong Han (Post-doctoral Fellow)
[Supervisor: Professor Pengtao Liu]

Conventional understanding dictates that mammalian neural stem cells (NSCs) exist only in the central nervous system (CNS). Here, we report that peripheral NSCs (pNSCs) exist outside of the CNS and can be isolated—from mouse embryonic limb, postnatal lung, tail, dorsal root ganglia, and adult lung tissues. Derived pNSCs are distinct from neural crest stem cells, express multiple NSC-specific markers and exhibit cell morphology, self-renewing and differentiation capacity, genome-wide transcriptional profile, and epigenetic features similar to control brain NSCs. pNSCs are composed of Sox1⁺ cells originating from neuroepithelial cells. pNSCs in situ have similar molecular features to NSCs in the brain. Furthermore, many pNSCs that migrate out of the neural tube can differentiate into mature neurons and limited glial cells during embryonic and postnatal development. Our discovery of pNSCs provides previously unidentified insight into the mammalian nervous system development and presents an alternative potential strategy for neural regenerative therapy.

Insights into diagnosis of metatranscript-only Titinopathy patients
Dr. Yanmin Zhang (Post-doctoral Fellow)
[Supervisor: Professor Asif Javed]

Titinopathy, or muscular dystrophy caused by defects in titin (TTN), pose a diagnostic challenge due to variability in patient symptoms and sheer size of the gene. Mutations in metatranscript-only exons in TTN are particularly difficult to interpret due to the complex isoform usage pattern of this locus. Recently a new subtype of recessive Titinopathy has been reported with patients having one (or both) disease variants within this locus. We report four new families with this condition which were solved after a decade long diagnostic odyssey thanks to a multi-omics approach. We will present a diagnostic framework to help future cases which were validated in an independent cohort. And conclude by sharing ongoing reprogramming work towards mechanistic understanding of this newly discovered recessive Titinopathy.

All are welcome.