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BCL-11 enables adaptive stress responses to environmental challenges
Patrizia Niedworok1,2, Rossella Erminia Ciliberti1, Beijia Xie1
1German Center for Neurodegenerative Diseases (DZNE), 53127 Bonn, Germany.
Iscience
|February 5, 2026
Summary
BCL-11 deficiency impairs stress resilience in insulin/IGF-1 signaling (IIS) pathways, particularly affecting Caenorhabditis elegans daf-2 mutants. BCL-11 is crucial for enhancing stress resistance in adult animals.
Area of Science:
- Cellular homeostasis
- Metabolism
- Stress resilience
Background:
- Insulin/IGF-1 signaling (IIS) is a key regulator of metabolism and stress response.
- DAF-2 and DAF-16/FOXO are central components of IIS in C. elegans.
- BCL-11 is an evolutionarily conserved transcription factor linked to human neurodevelopmental disorders.
Purpose of the Study:
- Investigate the role of BCL-11 in IIS pathways.
- Determine how pathogenic BCL-11 variants affect C. elegans development and stress response.
- Elucidate the interaction between BCL-11 and DAF-16 in IIS-deficient animals.
Main Methods:
- Utilized Caenorhabditis elegans as a model organism.
- Generated and analyzed hypomorphic bcl-11 mutations.
- Assessed the impact of bcl-11 deficiency on daf-2 signaling under standard and stress conditions.
- Examined egg hatching defects and transcriptional interplay using daf-16 loss-of-function.
Main Results:
- Hypomorphic bcl-11 mutations had minimal effects on C. elegans growth and survival under normal conditions.
- BCL-11 deficiency compromised the stress-protective functions of daf-2 signaling.
- Loss of daf-16 rescued embryonic lethality in daf-2;bcl-11 mutants, indicating a transcriptional interaction.
- BCL-11 plays a role in transcriptional regulation during development and stress response.
Conclusions:
- BCL-11 actively regulates transcription during development.
- In adult animals, BCL-11 is recruited upon environmental insult to bolster stress resilience.
- BCL-11 is a critical modulator of IIS-mediated stress adaptation.
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