Date: Wednesday, 20 October 2021

Venue: Cheung Kung Hai Lecture Theatre 3, 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: Dr. Ka Kui TONG (Post-doctoral Fellow)
Primary Supervisor: Prof. Danny CHAN
Presentation Title: The roles of Irx3 and Irx5 in epithelial-neural crest interaction during craniofacial morphogenesis
Abstract: Craniofacial malformation is a common human congenital disorder, which severely affects daily life. Being a complex organ, craniofacial morphogenesis requires coordination of multiple cell types and signaling. Mutations of IRX5 gene, a homeodomain transcription factor, cause Hamamy syndrome: multiple craniofacial defects including jaw abnormalities. However, the roles of Irx genes in craniofacial development are not known. Here, we observed jaw morphogenetic defects in a series of Irx3 and Irx5 (Irx3/5) mutant mice. As the jaw are derived from the neural crest cells of the first pharyngeal arch (PA1), early patterning malformations were found. However, Wnt1-Cre driven Irx mutants showed much milder phenotypes, suggesting non-cell autonomous requirement of Irx3/5. Using scRNA-seq analyses, we investigated the roles of Irx3/5 in regulating the signaling interaction between PA1 epithelium and the surrounding neural crests. Through this study, we provide mechanistic model to explain early pattern of the jaw.

5:30 p.m. 

Speaker: Dr. Yun CHENG (Post-doctoral Fellow)
Primary Supervisor: Prof. Dong-Yan JIN
Presentation Title: FACI is a novel fasting- and CREB-H-induced protein that inhibits intestinal lipid absorption and reverses diet-induced obesity
Abstract: CREB-H is a key transcription factor governing lipid metabolism. In search of CREB-H targets, here we identified a novel fasting- and CREB-H-induced (FACI) protein that inhibits intestinal lipid absorption and alleviates diet-induced obesity in mice. FACI expression was enriched in liver and intestine. FACI is a phospholipid-binding protein that localizes to plasma membrane and recycling endosomes. The transcription of Faci was regulated by not only CREB-H, but also nutrient-responsive transcription factors SREBP1, HNF4α, PGC1α and CREB, as well as fasting-related cAMP signaling. Genetic knockout of Faci in mice displayed an increase in intestinal fat absorption. In accordance with this, Faci deficiency aggravated high-fat diet-induced obesity, insulin resistance and other obesity-related metabolic dysfunction in mice. Taken together, FACI is a novel fasting- and CREB-H-induced protein. Genetic disruption of Faci in mice revealed its inhibitory effect on fat absorption and obesity. Our findings shed light on a new target of CREB-H implicated in lipid homeostasis.

ALL ARE WELCOME

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