Date of Award


Document Type

Masters Thesis

Degree Name


Organizational Unit

College of Natural Science and Mathematics, Biological Sciences

First Advisor

Ann Wehman

Second Advisor

J. Todd Blankenship

Third Advisor

Cedric Asensio


ATG-16, Cell corpse, LC3-associated phagocytosis, Macroautophagy, Membrane breakdown, Polar body


Failure to digest cell corpses can lead to lupus-like autoimmune disorders in mammals. To better understand if LC3-associated phagocytosis (LAP) drives cell corpse breakdown in phagolysosomes, we studied the clearance of the C. elegans polar body during embryonic development. ATG16L1 has separable roles in regulating LC3 recruitment during macroautophagy and LAP. We demonstrated that the ATG16L1 C. elegans orthologs, ATG-16.1 and ATG-16.2, function redundantly to promote polar body membrane breakdown. We also discovered that truncating the LAP-specific WD40 domain of ATG-16.2 unexpectedly disrupts autophagy. Furthermore, we confirmed that polar body membrane breakdown occurs independent of macroautophagy. We also showed that LC3 localizes to the phagolysosome independent of autophagosomes. Although these findings show macroautophagy is unlikely to be promoting polar body degradation, the mechanism by which LC3 is recruited to the polar body phagolysosome to promote cell corpse breakdown remains unknown.

Copyright Date


Copyright Statement / License for Reuse

All Rights Reserved
All Rights Reserved.

Publication Statement

Copyright is held by the author. User is responsible for all copyright compliance.

Rights Holder

Shruti Kolli


Received from ProQuest

File Format



English (eng)


81 pgs

File Size

3.6 MB


Molecular biology, Cellular biology, Biology

Available for download on Friday, September 12, 2025