Digital Public Defence: Kia Wee Tan
MSc Kia Wee Tan at Institute of Clinical Medicine will be defending the thesis “Membrane Remodeling in Macropinocytosis” for the degree of PhD (Philosophiae Doctor).
Photo: Chema Bassols
The public defence will be held as a video conference over Zoom.
The defence will follow regular procedure as far as possible, hence it will be open to the public and the audience can ask ex auditorio questions when invited to do so.
Due to copyright reasons, an electronic copy of the thesis must be ordered from the faculty. In order for the faculty to have time to process the order, it must be received by the faculty no later than 2 days prior to the public defence. Orders received later than 2 days before the defence will not be processed. Inquiries regarding the thesis after the public defence must be addressed to the candidate.
Digital Trial Lecture – time and place
- First opponent: Professor Laura Machesky, Beatson Institute for Cancer Research, UK
- Second opponent: Principal Investigator Jason King, Department of Biomedical Sciences, University of Sheffield, UK
- Third member and chair of the evaluation committee: Professor Therese Sørlie, University of Oslo
Chair of the Defence
Associate Professor Ragnhild Eskeland, University of Oslo
Project leader Kay Schink, CanCell, Centre for Cancer Cell Reprogramming
Macropinocytosis is an actin-driven bulk endocytosis pathway that internalizes extracellular material into large intracellular vesicles called macropinosomes. This form of endocytosis is found in many cell types and serves many different roles, from nutrient intake to regulation of cell surface proteins. While some parts of this process have been elucidated, many aspects of the molecular machinery that are involved in macropinocytosis still remain to be understood. This dissertation by Kia Wee Tan concerns the role of two proteins (Phafin2 and JIP4) that coordinate membrane trafficking at macropinosomes.
Newly formed macropinosomes contain a lipid composition that allows Phafin2 to recognise and localize to their membranes. Phafin2 is capable of binding to polymerized actin (F-actin) and appears to perturb actin dynamics at membranes. Because the loss of Phafin2 impairs macropinocytosis at a stage where the new macropinosome is still coated in actin, we propose that Phafin2 assists in uncoating the macropinosome from a “shell” of actin, allowing it to fully mature into an endosome-like vesicle.
Once the macropinosome has matured into an endosome-like vesicle, a process called endocytic recycling takes place, where its cargo is sorted into recycling and degradative pathways. Cargo to be recycled away from the macropinosome is concentrated into membrane tubules formed from the vesicle membrane and detached. JIP4 assists in the formation of these tubules, and it uses Phafin2 as an adapter to localize to macropinosomes. The loss of JIP4 causes accumulation of macropinocytosed cargo, and thus it is important for efficient recycling out from the macropinosome.
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