Related Experiment Video
Updated: Jun 21, 2026
Live Imaging Followed by Single Cell Tracking to Monitor Cell Biology and the Lineage Progression of Multiple Neural Populations
Published on: December 16, 2017
Lgl antagonizes Par complex membrane association to enable neural stem cell asymmetric division
Sarah E Welch1, Bryce LaFoya1, Kenneth E Prehoda1
1Institute of Molecular Biology, Department of Chemistry and Biochemistry, 1229 University of Oregon, Eugene, OR 97403, USA.
Abstract:
The Par complex regulates cell polarity in diverse animal cells, but how it is restricted to a specific membrane domain remains unclear. The tumor suppressor Lethal giant larvae (Lgl) is thought to inhibit Par complex membrane binding, yet in metaphase Drosophila neural stem cells (NSCs), Lgl is cytoplasmic while the Par complex is apically polarized, raising the question of how Lgl controls Par localization when it is not on the membrane. Using live imaging, we found that Lgl and atypical Protein Kinase C (aPKC) exhibit tightly coordinated, opposing membrane dynamics: aPKC displaces Lgl at mitotic entry, while Lgl displaces aPKC at mitotic exit. In Lgl-depleted NSCs, aPKC is not fully cleared from the membrane after mitosis, and this residual aPKC persists into the subsequent division, disrupting Miranda polarization. Apical aPKC recruitment still occurs, indicating that Lgl is not required for Par polarization per se, but rather for ensuring aPKC absence from the basal membrane before mitosis. These findings reveal a temporal mode of mutual antagonism between Lgl and the Par complex that may license proper asymmetric division.
Insights
Lethal giant larvae (Lgl) protein and the Par complex dynamically regulate cell polarity by mutually antagonizing each other during cell division. This ensures proper asymmetric cell division in Drosophila neural stem cells.
Area of Science:
- Cell Biology
- Developmental Biology
- Neuroscience
Background:
- The Par complex is crucial for establishing cell polarity in various animal cells.
- The tumor suppressor Lethal giant larvae (Lgl) is hypothesized to inhibit Par complex membrane binding.
- The localization of Lgl and the Par complex in metaphase Drosophila neural stem cells (NSCs) presents a paradox regarding Lgl's inhibitory role.
Purpose of the Study:
- To investigate how Lethal giant larvae (Lgl) controls Par complex localization in Drosophila neural stem cells (NSCs) when Lgl is not membrane-bound.
- To elucidate the dynamic relationship between Lgl and the Par complex during cell division.
- To understand the mechanism ensuring proper asymmetric cell division.
Main Methods:
- Live imaging of Drosophila neural stem cells (NSCs).
- Depletion of Lgl to observe effects on Par complex localization.
- Analysis of protein dynamics at the cell membrane during mitosis.
Main Results:
- Lethal giant larvae (Lgl) and atypical Protein Kinase C (aPKC) exhibit coordinated, opposing membrane dynamics: aPKC displaces Lgl at mitotic entry, and Lgl displaces aPKC at mitotic exit.
- In Lgl-depleted NSCs, residual aPKC persists on the membrane post-mitosis, disrupting Miranda polarization in subsequent divisions.
- Lgl is not essential for apical aPKC recruitment but ensures basal membrane clearance before mitosis.
Conclusions:
- A temporal mode of mutual antagonism exists between Lgl and the Par complex.
- This antagonism is critical for regulating Par complex localization and ensuring proper asymmetric cell division.
- Lgl's role in clearing aPKC from the basal membrane is vital for subsequent cell divisions.
More Related Videos
11:52Establishment of an Electrophysiological Platform for Modeling ALS with Regionally-Specific Human Pluripotent Stem Cell-Derived Astrocytes and Neurons
Published on: August 26, 2021
09:06Antibody Uptake Assay for Tracking Notch/Delta Endocytosis During the Asymmetric Division of Zebrafish Radial Glia Progenitors
Published on: January 20, 2023
