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The autism susceptibility kinase, TAOK2, phosphorylates eEF2 and modulates translation

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The autism susceptibility kinase, TAOK2, phosphorylates eEF2 and modulates translation. / Henis, Melad; Rücker, Tabitha; Scharrenberg, Robin; Richter, Melanie; Baltussen, Lucas; Hong, Shuai; Meka, Durga Praveen; Schwanke, Birgit; Neelagandan, Nagammal; Daaboul, Danie; Murtaza, Nadeem; Krisp, Christoph; Harder, Sönke; Schlüter, Hartmut; Kneussel, Matthias; Hermans-Borgmeyer, Irm; de Wit, Joris; Singh, Karun K; Duncan, Kent E; de Anda, Froylan Calderón.

In: SCI ADV, Vol. 10, No. 15, 12.04.2024, p. eadf7001.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Henis, M, Rücker, T, Scharrenberg, R, Richter, M, Baltussen, L, Hong, S, Meka, DP, Schwanke, B, Neelagandan, N, Daaboul, D, Murtaza, N, Krisp, C, Harder, S, Schlüter, H, Kneussel, M, Hermans-Borgmeyer, I, de Wit, J, Singh, KK, Duncan, KE & de Anda, FC 2024, 'The autism susceptibility kinase, TAOK2, phosphorylates eEF2 and modulates translation', SCI ADV, vol. 10, no. 15, pp. eadf7001. https://doi.org/10.1126/sciadv.adf7001

APA

Henis, M., Rücker, T., Scharrenberg, R., Richter, M., Baltussen, L., Hong, S., Meka, D. P., Schwanke, B., Neelagandan, N., Daaboul, D., Murtaza, N., Krisp, C., Harder, S., Schlüter, H., Kneussel, M., Hermans-Borgmeyer, I., de Wit, J., Singh, K. K., Duncan, K. E., & de Anda, F. C. (2024). The autism susceptibility kinase, TAOK2, phosphorylates eEF2 and modulates translation. SCI ADV, 10(15), eadf7001. https://doi.org/10.1126/sciadv.adf7001

Vancouver

Henis M, Rücker T, Scharrenberg R, Richter M, Baltussen L, Hong S et al. The autism susceptibility kinase, TAOK2, phosphorylates eEF2 and modulates translation. SCI ADV. 2024 Apr 12;10(15):eadf7001. https://doi.org/10.1126/sciadv.adf7001

Bibtex

@article{33671eec4812495b939d83c3a39f939c,
title = "The autism susceptibility kinase, TAOK2, phosphorylates eEF2 and modulates translation",
abstract = "Genes implicated in translation control have been associated with autism spectrum disorders (ASDs). However, some important genetic causes of autism, including the 16p11.2 microdeletion, bear no obvious connection to translation. Here, we use proteomics, genetics, and translation assays in cultured cells and mouse brain to reveal altered translation mediated by loss of the kinase TAOK2 in 16p11.2 deletion models. We show that TAOK2 associates with the translational machinery and functions as a translational brake by phosphorylating eukaryotic elongation factor 2 (eEF2). Previously, all signal-mediated regulation of translation elongation via eEF2 phosphorylation was believed to be mediated by a single kinase, eEF2K. However, we show that TAOK2 can directly phosphorylate eEF2 on the same regulatory site, but functions independently of eEF2K signaling. Collectively, our results reveal an eEF2K-independent signaling pathway for control of translation elongation and suggest altered translation as a molecular component in the etiology of some forms of ASD.",
author = "Melad Henis and Tabitha R{\"u}cker and Robin Scharrenberg and Melanie Richter and Lucas Baltussen and Shuai Hong and Meka, {Durga Praveen} and Birgit Schwanke and Nagammal Neelagandan and Danie Daaboul and Nadeem Murtaza and Christoph Krisp and S{\"o}nke Harder and Hartmut Schl{\"u}ter and Matthias Kneussel and Irm Hermans-Borgmeyer and {de Wit}, Joris and Singh, {Karun K} and Duncan, {Kent E} and {de Anda}, {Froylan Calder{\'o}n}",
year = "2024",
month = apr,
day = "12",
doi = "10.1126/sciadv.adf7001",
language = "English",
volume = "10",
pages = "eadf7001",
journal = "SCI ADV",
issn = "2375-2548",
publisher = "American Association for the Advancement of Science",
number = "15",

}

RIS

TY - JOUR

T1 - The autism susceptibility kinase, TAOK2, phosphorylates eEF2 and modulates translation

AU - Henis, Melad

AU - Rücker, Tabitha

AU - Scharrenberg, Robin

AU - Richter, Melanie

AU - Baltussen, Lucas

AU - Hong, Shuai

AU - Meka, Durga Praveen

AU - Schwanke, Birgit

AU - Neelagandan, Nagammal

AU - Daaboul, Danie

AU - Murtaza, Nadeem

AU - Krisp, Christoph

AU - Harder, Sönke

AU - Schlüter, Hartmut

AU - Kneussel, Matthias

AU - Hermans-Borgmeyer, Irm

AU - de Wit, Joris

AU - Singh, Karun K

AU - Duncan, Kent E

AU - de Anda, Froylan Calderón

PY - 2024/4/12

Y1 - 2024/4/12

N2 - Genes implicated in translation control have been associated with autism spectrum disorders (ASDs). However, some important genetic causes of autism, including the 16p11.2 microdeletion, bear no obvious connection to translation. Here, we use proteomics, genetics, and translation assays in cultured cells and mouse brain to reveal altered translation mediated by loss of the kinase TAOK2 in 16p11.2 deletion models. We show that TAOK2 associates with the translational machinery and functions as a translational brake by phosphorylating eukaryotic elongation factor 2 (eEF2). Previously, all signal-mediated regulation of translation elongation via eEF2 phosphorylation was believed to be mediated by a single kinase, eEF2K. However, we show that TAOK2 can directly phosphorylate eEF2 on the same regulatory site, but functions independently of eEF2K signaling. Collectively, our results reveal an eEF2K-independent signaling pathway for control of translation elongation and suggest altered translation as a molecular component in the etiology of some forms of ASD.

AB - Genes implicated in translation control have been associated with autism spectrum disorders (ASDs). However, some important genetic causes of autism, including the 16p11.2 microdeletion, bear no obvious connection to translation. Here, we use proteomics, genetics, and translation assays in cultured cells and mouse brain to reveal altered translation mediated by loss of the kinase TAOK2 in 16p11.2 deletion models. We show that TAOK2 associates with the translational machinery and functions as a translational brake by phosphorylating eukaryotic elongation factor 2 (eEF2). Previously, all signal-mediated regulation of translation elongation via eEF2 phosphorylation was believed to be mediated by a single kinase, eEF2K. However, we show that TAOK2 can directly phosphorylate eEF2 on the same regulatory site, but functions independently of eEF2K signaling. Collectively, our results reveal an eEF2K-independent signaling pathway for control of translation elongation and suggest altered translation as a molecular component in the etiology of some forms of ASD.

U2 - 10.1126/sciadv.adf7001

DO - 10.1126/sciadv.adf7001

M3 - SCORING: Journal article

C2 - 38608030

VL - 10

SP - eadf7001

JO - SCI ADV

JF - SCI ADV

SN - 2375-2548

IS - 15

ER -