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Updated: Jun 1, 2026
Visualizing Neuroblast Cytokinesis During C. elegans Embryogenesis
Published on: March 12, 2014
The Arf GAP CNT-2 regulates the apoptotic fate in C. elegans asymmetric neuroblast divisions
Aakanksha Singhvi1, Jerome Teuliere, Karla Talavera
1Department of Molecular and Cell Biology and Helen Wills Neuroscience Institute, University of California, Berkeley, Berkeley, CA 94720, USA.
Abstract:
During development, all cells make the decision to live or die. Although the molecular mechanisms that execute the apoptotic program are well defined, less is known about how cells decide whether to live or die. In C. elegans, this decision is linked to how cells divide asymmetrically [1, 2]. Several classes of molecules are known to regulate asymmetric cell divisions in metazoans, yet these molecules do not appear to control C. elegans divisions that produce apoptotic cells [3]. We identified CNT-2, an Arf GTPase-activating protein (GAP) of the AGAP family, as a novel regulator of this type of neuroblast division. Loss of CNT-2 alters daughter cell size and causes the apoptotic cell to adopt the fate of its sister cell, resulting in extra neurons. CNT-2's Arf GAP activity is essential for its function in these divisions. The N terminus of CNT-2, which contains a GTPase-like domain that defines the AGAP class of Arf GAPs, negatively regulates CNT-2's function. We provide evidence that CNT-2 regulates receptor-mediated endocytosis and consider the implications of its role in asymmetric cell divisions.
Insights
Researchers discovered CNT-2, a novel regulator of asymmetric cell division in C. elegans neuroblasts. Loss of CNT-2 leads to extra neurons by altering cell size and fate decisions during development.
Area of Science:
- Cell biology
- Developmental biology
- Neuroscience
Background:
- Cellular decisions to live or die are crucial during development.
- While apoptotic mechanisms are known, the decision-making process is less understood.
- In C. elegans, asymmetric cell division is linked to cell death decisions.
Purpose of the Study:
- To identify novel regulators of asymmetric neuroblast divisions that produce apoptotic cells in C. elegans.
- To elucidate the function and mechanism of CNT-2 in these developmental processes.
Main Methods:
- Genetic screening in C. elegans to identify regulators of neuroblast division.
- Analysis of cell size, cell fate, and neuronal number in CNT-2 loss-of-function mutants.
- Biochemical assays to assess the GTPase-activating protein (GAP) activity of CNT-2.
Main Results:
- CNT-2, an Arf GTPase-activating protein (GAP) of the AGAP family, was identified as a novel regulator.
- Loss of CNT-2 function resulted in altered daughter cell size and the apoptotic cell adopting its sister's fate, leading to supernumerary neurons.
- CNT-2's Arf GAP activity is essential for its role, and its N-terminal domain negatively regulates its function.
Conclusions:
- CNT-2 plays a critical role in regulating asymmetric neuroblast divisions and cell fate decisions in C. elegans.
- The findings suggest CNT-2 regulates receptor-mediated endocytosis, impacting developmental outcomes.
- CNT-2 represents a new target for understanding the molecular control of cell death and neuronal development.
