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Journal Article

Stress-induced nuclear condensation of NELF drives transcriptional downregulation

MPS-Authors

Rawat,  Prashant
Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Hummel,  Barbara
Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Aprile-Garcia,  Fernando
Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Pandit,  Anwit S
Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Eisenhardt,  Nathalie
Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Khavaran,  Ashkan
Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Pichler,  Andrea
Department of Epigenetics, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Sawarkar,  Ritwick
Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Rawat et al. 2021.pdf
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Citation

Rawat, P., Boehning, M., Hummel, B., Aprile-Garcia, F., Pandit, A. S., Eisenhardt, N., et al. (2021). Stress-induced nuclear condensation of NELF drives transcriptional downregulation. Molecular Cell, 81, 1-14. doi:10.1016/j.molcel.2021.01.016.


Cite as: http://hdl.handle.net/21.11116/0000-0007-E985-C
Abstract
In response to stress, human cells coordinately downregulate transcription and translation of housekeeping genes. To downregulate transcription, the negative elongation factor (NELF) is recruited to gene promoters impairing RNA polymerase II elongation. Here we report that NELF rapidly forms nuclear condensates upon stress in human cells. Condensate formation requires NELF dephosphorylation and SUMOylation induced by stress. The intrinsically disordered region (IDR) in NELFA is necessary for nuclear NELF condensation and can be functionally replaced by the IDR of FUS or EWSR1 protein. We find that biomolecular condensation facilitates enhanced recruitment of NELF to promoters upon stress to drive transcriptional downregulation. Importantly, NELF condensation is required for cellular viability under stressful conditions. We propose that stress-induced NELF condensates reported here are nuclear counterparts of cytosolic stress granules. These two stress-inducible condensates may drive the coordinated downregulation of transcription and translation, likely forming a critical node of the stress survival strategy.