BYU

Abstract by Misael Lazaro

Personal Infomation


Presenter's Name

Misael Lazaro

Degree Level

Undergraduate

Abstract Infomation


Department

Chemistry and Biochemistry

Faculty Advisor

Joshua Andersen

Title

ATG9A and ULK1 mechanisms in Autophagy

Abstract

Autophagy is a degradation pathway among eukaryotes that cleans out damaged organelles in order to regenerate new ones. Vesicles called autophagosomes carry the broken-down organelles to the lysosome for degradation. This life preserving mechanism can also enable tumor cell survival by providing nutrients even under chemotherapy conditions. ATG9A is known to deliver membrane tissue to the autophagosome formation site (PAS) where it then interacts with the intricate ULK1 complex. The ULK1 complex is the central regulator for autophagosome growth thought to recruit ATG proteins to the PAS. However, the regulatory mechanisms of ATG9A and ULK1 complex are poorly understood. Through BioID, we identified ATG9A C-terminal interactions that include members of the ULK1 complex. Furthermore, via co-immunoprecipitations we find that ATG9A interacts with an ATG13 subcomplex apart from the canonical ULK1 complex. By further understanding of these mechanisms, we can create therapeutic treatments for chemo resistant cancers.