NMY-2, TOE-2 and PIG-1 regulate Caenorhabditis elegans asymmetric cell divisions
Joseph Robinson1, Jerome Teuliere1, Shinja Yoo1
1Department of Molecular and Cell Biology, University of California Berkeley, Berkeley, CA, United States of America.
Plos One
|May 24, 2024
Summary
In C. elegans development, Daughter Cell Size Asymmetry (DCSA) is crucial. This study reveals that NMY-2 protein influences cell fate determination independently of its role in DCSA during neuroblast divisions.
Area of Science:
- Cell Biology
- Developmental Biology
- Genetics
Background:
- Asymmetric cell division generates cellular diversity.
- Daughter Cell Size Asymmetry (DCSA) produces daughters of different sizes, with the smaller one often undergoing apoptosis.
- In C. elegans, Q.a and Q.p neuroblast divisions exhibit DCSA, producing larger survivors and smaller apoptotic cells.
Purpose of the Study:
- To investigate the roles of NMY-2, TOE-2, and PIG-1 in regulating DCSA during Q.a and Q.p neuroblast divisions.
- To characterize the cortical localization of NMY-2, TOE-2, and PIG-1 during these asymmetric divisions.
- To determine the function of NMY-2 in DCSA and cell fate determination.
Main Methods:
- Utilized endogenously tagged NMY-2, TOE-2, and PIG-1 reporters to visualize protein localization.
- Employed temperature-sensitive nmy-2 mutants to assess the role of NMY-2 in DCSA.
- Generated double mutant combinations (nmy-2 with toe-2 and pig-1) to analyze genetic interactions.
Main Results:
- TOE-2 localized to the smaller daughter pole, PIG-1 to the larger daughter pole in both Q.a and Q.p divisions.
- NMY-2 localized to the smaller daughter pole in Q.a but not asymmetrically in Q.p.
- nmy-2 mutants exhibited DCSA defects specifically in Q.p divisions.
- nmy-2 mutations did not significantly alter DCSA defects in toe-2 and pig-1 mutants but affected daughter cell numbers, suggesting an independent role in cell fate.
Conclusions:
- NMY-2 plays a critical role in specifying cell fates of Q.a and Q.p neuroblasts, separate from its function in DCSA.
- Differential localization of TOE-2 and PIG-1 contributes to DCSA in both Q.a and Q.p divisions.
- NMY-2's role in DCSA is division-specific, being essential for Q.p but not Q.a, yet it impacts cell fate in both.
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