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Producing Gene Deletions in Escherichia coli by P1 Transduction with Excisable Antibiotic Resistance Cassettes
Published on: September 1, 2018
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Vav-iCre-Mediated Deletion of TFAM Is Not Recoverable and Is Consistent with Embryonic Lethality
Rituparna Ghosh1, Elina Shakur1, Matthew J Yousefzadeh1
1Columbia Center for Translational Immunology and Burch-Lodge Center for Human Longevity, Department of Medicine, Columbia University Medical Center, New York, NY 10032, USA.
Genes
|March 28, 2026
Summary
Mitochondrial genome instability accelerates aging. Loss of TFAM in immune cells caused embryonic lethality, while SIRT6 deficiency was viable, highlighting the critical role of mitochondrial DNA maintenance in immunity.
Area of Science:
- Immunology
- Genetics
- Aging Research
Background:
- Genome stability is crucial for cellular health, preventing aging, cancer, and disease.
- DNA damage drives cellular senescence and mitochondrial dysfunction, key aging factors.
- Instability in nuclear and mitochondrial genomes contributes to aging, impacting the hematopoietic system and beyond.
Purpose of the Study:
- To investigate the impact of TFAM loss in all immune cells on the immune system and parenchyma.
- To compare the effects of TFAM deficiency with SIRT6 deficiency in immune cells.
Main Methods:
- Attempted generation of Vav-iCre+/-; Tfamfl/fl mice lacking TFAM in all immune cells.
- Generated mice lacking SIRT6 in all immune cells.
Main Results:
- Vav-iCre+/-; Tfamfl/fl mice were unrecoverable, indicating embryonic lethality.
- Mice lacking SIRT6 in all immune cells were viable and born at Mendelian frequencies.
Conclusions:
- Mitochondrial genome maintenance is essential for immune system function.
- TFAM deficiency in immune cells leads to embryonic lethality, underscoring its critical role.
- SIRT6 plays a vital role in immune homeostasis, with its deficiency not causing lethality.
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