Date: Wednesday, 21 September 2022

Time: 5:00 p.m. - 6:00 p.m.

Venue: Room 2 & 3, G/F, William M.W. Mong Block, 21 Sassoon Road

5:00 p.m.

Speaker: Dr. Sin Guang CHEN (Post-doctoral Fellow)
Primary Supervisor: Dr. Alan WONG
Presentation Title: Generation of genetically modified mice using RNA-guided base editing in mouse embryos
Abstract: Cytosine base editors (CBEs) composed of an engineered cytosine deaminase and the Streptococcus pyogenes Cas9 nickase enable C-to-T single-nucleotide substitutions in a single guide RNA (sgRNA)-dependent manner. We aim to set up the platform for generating gene-modified mice with single-nucleotide substitutions using CBEs. We will design sgRNAs that create a premature stop codon by a single C-to-T conversion at the target site in each gene. We will conduct the editing in mouse embryos by microinjection of CBE-encoding mRNA and sgRNAs, or CBE- and sgRNA-encoding plasmids. To optimize the methods and experimental parameters, we will use CBEs to induce nonsense mutations in two example mouse genes, Foxn1 and Tyr, which encode forkhead box protein N1 and tyrosinase. Mutations in Foxn1 cause inborn thymic dysgenesis and hairless skin. The Tyr gene mutation causes a complete loss of pigmentation (albinism). This study will set up the application of CBEs in creating transgenic animals.

5:30 p.m. 

Speaker: Dr. Siwen LI  (Post-doctoral Fellow)
Primary Supervisor: Dr. You-qiang SONG
Presentation Title: MicroRNA-128 suppresses tau phosphorylation and reduces amyloid-beta accumulation by inhibiting the expression of GSK3beta, APPBP2, and mTOR in Alzheimer’s disease
Abstract: Alzheimer’s disease (AD) is the most common form of dementia in older adults. Recent studies have shown that many microRNAs (miRNAs) are dysregulated in AD, and modulation of these dysregulated miRNAs can counteract AD neuropathology. MicroRNA-128 (miR-128) is expressed in the brain and dysregulated in AD. However, the functional roles of miR-128 in AD has not been fully examined. Herein, we found that miR-128 suppressed tau phosphorylation and Aβ secretion in AD cellular models, and alleviated cognitive decline and reduced plaque deposition in AD transgenic 5XFAD mice. Mechanistically, miR-128 exerted suppressive effects by directly repressing the expression of GSK3β, APPBP2, and mTOR. Our study findings suggest miR-128 could serve as a molecular target for drug development for AD. We also find a possible mechanism underlying the dysregulation of miR-128 in AD, in which Aβ reduces miR-128 expression by inhibiting C/EBPα.

ALL ARE WELCOME

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