School of Science Division of Life Science 22 Molecular Regulation of Axon Regeneration Supervisor: LIU Kai / LIFS Student: LIU Jingyi / BIBU Course: UROP1100, Fall The adult mammalian central nervous system's (CNS) failure to regenerate axons is linked to two features of the CNS: a restrictive extrinsic environment and a decreased intrinsic regenerative capacity of mature CNS neurons. The goal of the research is to find and analyze new genes involved in axon regeneration, particularly those that are regulated intrinsically. Inability of the injured axon to regenerate and rebuild their function is a fatal problem after central nervous system injury. Even if they sometimes regenerate, it is almost impossible for them to connect with its original target. In contrast, strong regeneration occurs after peripheral nerve injury, which can lead to the recovery of sensory and motor functions. Molecular Regulation of Axon Regeneration Supervisor: LIU Kai / LIFS Student: TAN Lianxing / IRE Course: UROP1000, Summer PC12 cell line derived from a pheochromocytoma of the rat adrenal medulla. It is one of the most used cell lines in neuroscience research, such as neuron secretion, toxicity, and axon regeneration due to its neuronal properties and ease of culture. We, therefore, tested a series of compounds using a PC12 cell line to mimic the effects of these compounds on normal neurons. And it was found that CP-105696, a Leukotriene B4 receptor (LTB4R) antagonist, significantly impacted PC12 neurite growth. By looking for downstream signals, several possibilities for this effect are suggested. The Rules of Packaging Fat in Cells Supervisor: MAK Ho Yi / LIFS Student: CHIU Chung Wah / SSCI Course: UROP1100, Summer Triacylglycerols (TAGs) are the main stores of metabolic energy and fatty acids in human body. Abnormalities in TAG biosynthesis could disrupt the lipid homeostasis. Two acyl-CoA diacylglycerol acyltransferase (DGAT) enzymes, DGAT1 and DGAT2 are identified to account for the vast majority of TAG biosynthesis in human. Although the C. elegans DGAT2 ortholog has been identified, the identity of the DGAT1 ortholog is unknown. Here we investigate the effects on C. elegans intestinal lipid droplet (LD) phenotype upon the deletion of a putative DGAT1 ortholog in C. elegans.