The DOI matches its Crossref record; 6 of the 6 references it cites were found in a registry or an index.
Metabolic maintenance of cell asymmetry following division in activated T lymphocytes
Open accessAbstract
Asymmetric cell division, the partitioning of cellular components in response to polarizing cues during mitosis, has roles in differentiation and development. It is important for the self-renewal of fertilized zygotes in Caenorhabditis elegans and neuroblasts in Drosophila, and in the development of mammalian nervous and digestive systems. T lymphocytes, upon activation by antigen-presenting cells (APCs), can undergo asymmetric cell division, wherein the daughter cell proximal to the APC is more likely to differentiate into an effector-like T cell and the distal daughter is more likely to differentiate into a memory-like T cell. Upon activation and before cell division, expression of the transcription factor c-Myc drives metabolic reprogramming, necessary for the subsequent proliferative burst. Here we find that during the first division of an activated T cell in mice, c-Myc can sort asymmetrically. Asymmetric distribution of amino acid transporters, amino acid content, and activity of mammalian target of rapamycin complex 1 (mTORC1) is correlated with c-Myc expression, and both amino acids and mTORC1 activity sustain the differences in c-Myc expression in one daughter cell compared to the other. Asymmetric c-Myc levels in daughter T cells affect proliferation, metabolism, and differentiation, and these effects are altered by experimental manipulation of mTORC1 activity or c-Myc expression. Therefore, metabolic signalling pathways cooperate with transcription programs to maintain differential cell fates following asymmetric T-cell division.
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Cites
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“As c-Myc regulates metabolic reprogramming during T cell activation 3, 16,17 , we tested whether metabolic differences exist in first-division T cells expressing high or low levels of c-Myc.”
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Cited by
mTOR Signaling in Growth, Metabolism, and Disease
Saxton, R. A., & Sabatini, D. M. (2017) · Cell · doi:10.1016/j.cell.2017.02.004 · Cited by 7,555
The PI3K Pathway in Human Disease
Fruman, D. A., Chiu, H., Hopkins, B. D., Bagrodia, S., Cantley, L. C., & Abraham, R. T. (2017) · Cell · doi:10.1016/j.cell.2017.07.029 · Cited by 2,749
The MYC oncogene — the grand orchestrator of cancer growth and immune evasion
Dhanasekaran, R., Deutzmann, A., Mahauad-Fernandez, W. D., Hansen, A. S., Gouw, A. M., & Felsher, D. W. (2022) · Nature Reviews Clinical Oncology · doi:10.1038/s41571-021-00549-2 · Cited by 986
Metabolic Regulation of T Cell Longevity and Function in Tumor Immunotherapy
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Glutathione primes t cell metabolism for inflammation
Mak, T. W., Grusdat, M., Duncan, G. S., Dostert, C., Nonnenmacher, Y., Cox, M., Binsfeld, C., Hao, Z., Brüstle, A., Itsumi, M., et al. (2017) · Immunity · doi:10.1016/j.immuni.2017.03.019 · Cited by 511
Metadata
- Authors
- Verbist, K. C., Guy, C. S., Milasta, S., Liedmann, S., Kamiński, M. M., Wang, R., & Green, D. R.
- Venue
- Nature
- Published
- 2016-04-11
- Volume
- 532
- Issue
- 7599
- Pages
- 389-393
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- OpenAlex
- W2319053438
- Cited by
- 275
- References
- 6
- FWCI
- 17.61
- Type
- journal article
- Language
- en
- Open access
- green
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- Verbist, K. C., Guy, C. S., Milasta, S., Liedmann, S., Kamiński, M. M., Wang, R., & Green, D. R. (2016). Metabolic maintenance of cell asymmetry following division in activated T lymphocytes. Nature. https://doi.org/10.1038/nature17442
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