Publication

DAF-16/FOXO and HLH-30/TFEB function as combinatorial transcription factors to promote stress resistance and longevity

Lin, X-X., Sen, I., Janssens, G. E., Zhou, X., Fonslow, B. R., Edgar, D., Stroustrup, N., Swoboda, P., Yates, J. R., Ruvkun, G. & Riedel, C. G., 23-Oct-2018, In : Nature Communications. 9, 15 p., 4400.

Research output: Contribution to journalArticleAcademicpeer-review

APA

Lin, X-X., Sen, I., Janssens, G. E., Zhou, X., Fonslow, B. R., Edgar, D., ... Riedel, C. G. (2018). DAF-16/FOXO and HLH-30/TFEB function as combinatorial transcription factors to promote stress resistance and longevity. Nature Communications, 9, [4400]. https://doi.org/10.1038/s41467-018-06624-0

Author

Lin, Xin-Xuan ; Sen, Ilke ; Janssens, Georges E. ; Zhou, Xin ; Fonslow, Bryan R. ; Edgar, Daniel ; Stroustrup, Nicholas ; Swoboda, Peter ; Yates, John R. ; Ruvkun, Gary ; Riedel, Christian G. / DAF-16/FOXO and HLH-30/TFEB function as combinatorial transcription factors to promote stress resistance and longevity. In: Nature Communications. 2018 ; Vol. 9.

Harvard

Lin, X-X, Sen, I, Janssens, GE, Zhou, X, Fonslow, BR, Edgar, D, Stroustrup, N, Swoboda, P, Yates, JR, Ruvkun, G & Riedel, CG 2018, 'DAF-16/FOXO and HLH-30/TFEB function as combinatorial transcription factors to promote stress resistance and longevity' Nature Communications, vol. 9, 4400. https://doi.org/10.1038/s41467-018-06624-0

Standard

DAF-16/FOXO and HLH-30/TFEB function as combinatorial transcription factors to promote stress resistance and longevity. / Lin, Xin-Xuan; Sen, Ilke; Janssens, Georges E.; Zhou, Xin; Fonslow, Bryan R.; Edgar, Daniel; Stroustrup, Nicholas; Swoboda, Peter; Yates, John R.; Ruvkun, Gary; Riedel, Christian G.

In: Nature Communications, Vol. 9, 4400, 23.10.2018.

Research output: Contribution to journalArticleAcademicpeer-review

Vancouver

Lin X-X, Sen I, Janssens GE, Zhou X, Fonslow BR, Edgar D et al. DAF-16/FOXO and HLH-30/TFEB function as combinatorial transcription factors to promote stress resistance and longevity. Nature Communications. 2018 Oct 23;9. 4400. https://doi.org/10.1038/s41467-018-06624-0


BibTeX

@article{6d57d4a0d5fd4c39acda7ccbead6d453,
title = "DAF-16/FOXO and HLH-30/TFEB function as combinatorial transcription factors to promote stress resistance and longevity",
abstract = "The ability to perceive and respond to harmful conditions is crucial for the survival of any organism. The transcription factor DAF-16/FOXO is central to these responses, relaying distress signals into the expression of stress resistance and longevity promoting genes. However, its sufficiency in fulfilling this complex task has remained unclear. Using C. elegans, we show that DAF-16 does not function alone but as part of a transcriptional regulatory module, together with the transcription factor HLH-30/TFEB. Under harmful conditions, both transcription factors translocate into the nucleus, where they often form a complex, co-occupy target promoters, and co-regulate many target genes. Interestingly though, their synergy is stimulus-dependent: They rely on each other, functioning in the same pathway, to promote longevity or resistance to oxidative stress, but they elicit heat stress responses independently, and they even oppose each other during dauer formation. We propose that this module of DAF-16 and HLH-30 acts by combinatorial gene regulation to relay distress signals into the expression of specific target gene sets, ensuring optimal survival under each given threat.",
keywords = "ELEGANS LIFE-SPAN, CAENORHABDITIS-ELEGANS, INHIBITION, METABOLISM, REGULATOR, AUTOPHAGY, REQUIRES, GENES, SEQ",
author = "Xin-Xuan Lin and Ilke Sen and Janssens, {Georges E.} and Xin Zhou and Fonslow, {Bryan R.} and Daniel Edgar and Nicholas Stroustrup and Peter Swoboda and Yates, {John R.} and Gary Ruvkun and Riedel, {Christian G.}",
year = "2018",
month = "10",
day = "23",
doi = "10.1038/s41467-018-06624-0",
language = "English",
volume = "9",
journal = "Nature Communications",
issn = "2041-1723",
publisher = "Nature Publishing Group",

}

RIS

TY - JOUR

T1 - DAF-16/FOXO and HLH-30/TFEB function as combinatorial transcription factors to promote stress resistance and longevity

AU - Lin, Xin-Xuan

AU - Sen, Ilke

AU - Janssens, Georges E.

AU - Zhou, Xin

AU - Fonslow, Bryan R.

AU - Edgar, Daniel

AU - Stroustrup, Nicholas

AU - Swoboda, Peter

AU - Yates, John R.

AU - Ruvkun, Gary

AU - Riedel, Christian G.

PY - 2018/10/23

Y1 - 2018/10/23

N2 - The ability to perceive and respond to harmful conditions is crucial for the survival of any organism. The transcription factor DAF-16/FOXO is central to these responses, relaying distress signals into the expression of stress resistance and longevity promoting genes. However, its sufficiency in fulfilling this complex task has remained unclear. Using C. elegans, we show that DAF-16 does not function alone but as part of a transcriptional regulatory module, together with the transcription factor HLH-30/TFEB. Under harmful conditions, both transcription factors translocate into the nucleus, where they often form a complex, co-occupy target promoters, and co-regulate many target genes. Interestingly though, their synergy is stimulus-dependent: They rely on each other, functioning in the same pathway, to promote longevity or resistance to oxidative stress, but they elicit heat stress responses independently, and they even oppose each other during dauer formation. We propose that this module of DAF-16 and HLH-30 acts by combinatorial gene regulation to relay distress signals into the expression of specific target gene sets, ensuring optimal survival under each given threat.

AB - The ability to perceive and respond to harmful conditions is crucial for the survival of any organism. The transcription factor DAF-16/FOXO is central to these responses, relaying distress signals into the expression of stress resistance and longevity promoting genes. However, its sufficiency in fulfilling this complex task has remained unclear. Using C. elegans, we show that DAF-16 does not function alone but as part of a transcriptional regulatory module, together with the transcription factor HLH-30/TFEB. Under harmful conditions, both transcription factors translocate into the nucleus, where they often form a complex, co-occupy target promoters, and co-regulate many target genes. Interestingly though, their synergy is stimulus-dependent: They rely on each other, functioning in the same pathway, to promote longevity or resistance to oxidative stress, but they elicit heat stress responses independently, and they even oppose each other during dauer formation. We propose that this module of DAF-16 and HLH-30 acts by combinatorial gene regulation to relay distress signals into the expression of specific target gene sets, ensuring optimal survival under each given threat.

KW - ELEGANS LIFE-SPAN

KW - CAENORHABDITIS-ELEGANS

KW - INHIBITION

KW - METABOLISM

KW - REGULATOR

KW - AUTOPHAGY

KW - REQUIRES

KW - GENES

KW - SEQ

U2 - 10.1038/s41467-018-06624-0

DO - 10.1038/s41467-018-06624-0

M3 - Article

VL - 9

JO - Nature Communications

JF - Nature Communications

SN - 2041-1723

M1 - 4400

ER -

ID: 77226207