Date: Friday, 25 February 2022

Time: 5:00 p.m. - 6:00 p.m.

Via Zoom: https://hku.zoom.us/j/97489738867?pwd=MFJVUmg3em9tY3ZWdUYyYXlJS0ZJZz09 

Meeting ID: 974 8973 8867

Password: 123544

5:00 p.m.

Presenter: Miss Huan CHEN, PhD candidate
Primary Supervisor: Prof. Jiandong HUANG
Presentation Title: Structural insights into Mycoplasma hyopneumoniae Lipoic acid ligase A
Abstract: Mycoplasma hyopneumoniae (Mhp) is the primary pathogen of swine enzootic pneumonia, leading to economic losses in swine industry. However, lack of study in Mhp pathogenic mechanisms have limited the development of effective vaccines and drugs. Previous studies indicated that Lipoic protein ligase is fundamental for growth of several microbials, such as E. coli. This enzyme can catalyze the formation of lipoyl-AMP from ATP and lipoic acid, and transfer the lipoate moiety to metabolic multienzyme complexes, such as the glycine cleavage system, etc. The lipoyl moiety act as an essential cofactor of those complexes. Although piles of studies have be established on Mhp since 1965, the lipoate metabolism pathway in Mhp remains unclear. In this study, two novel genes, namely LplA and LplJ, related in Mhp lipoic acid metabolism have been identified and investigated.

5:30 p.m.

Presenter: Mr. Yi ZHANG, PhD candidate
Primary Supervisor: Dr. You-qiang SONG
Presentation Title: Cell cycle associated transcription factors regulate neuroinflammation in Alzheimer's disease
Abstract: Alzheimer's disease (AD), the most common neurodegenerative disease, is the dominant cause of dementia. Rare variants of triggering receptor expressed on myeloid cells-2 (Trem2) remarkably causes higher risk of developing AD, suggesting the crucial role of microglia mediated neuroinflammation in the pathogenesis of the disease. In this study, through chromatin immunopreciptation, we identified several transcription factors (Pax6, c-Myb, E2F1) downstream of cell cycle which are responsible for transcriptional regulation of Trem2. In a cellular model of microglia cell line, we hypothesize that upon amyloid beta challenge, the cell cycle-related transcription factors are upregulated at both mRNA and protein level, which subsequently inhibit the expression of Trem2 and associated scavenging mechanisms which remove amyloid beta, thus blocking the turnover causing excessive extracellular accumulation. More importantly, these transcription factors also bind promoters of multiple pro-inflammatory cytokines, suggesting that they might play an essential role in neuroinflammation.

ALL ARE WELCOME

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