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WNT signalling control by KDM5C during development affects cognition

WNT signalling control by KDM5C during development affects cognition
WNT signalling control by KDM5C during development affects cognition
Although KDM5C is one of the most frequently mutated genes in X-linked intellectual disability1, the exact mechanisms that lead to cognitive impairment remain unknown. Here we use human patient-derived induced pluripotent stem cells and Kdm5c knockout mice to conduct cellular, transcriptomic, chromatin and behavioural studies. KDM5C is identified as a safeguard to ensure that neurodevelopment occurs at an appropriate timescale, the disruption of which leads to intellectual disability. Specifically, there is a developmental window during which KDM5C directly controls WNT output to regulate the timely transition of primary to intermediate progenitor cells and consequently neurogenesis. Treatment with WNT signalling modulators at specific times reveal that only a transient alteration of the canonical WNT signalling pathway is sufficient to rescue the transcriptomic and chromatin landscapes in patient-derived cells and to induce these changes in wild-type cells. Notably, WNT inhibition during this developmental period also rescues behavioural changes of Kdm5c knockout mice. Conversely, a single injection of WNT3A into the brains of wild-type embryonic mice cause anxiety and memory alterations. Our work identifies KDM5C as a crucial sentinel for neurodevelopment and sheds new light on KDM5C mutation-associated intellectual disability. The results also increase our general understanding of memory and anxiety formation, with the identification of WNT functioning in a transient nature to affect long-lasting cognitive function.
0028-0836
594-603
Karwacki-Neisius, Violetta
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Jang, Ahram
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Cukuroglu, Engin
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Tai, Albert
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Jiao, Alan
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Predes, Danilo
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Yoon, Joon
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Brookes, Emily
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Chen, Jiekai
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Iberg, Aimee
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Halbritter, Florian
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Õunap, Katrin
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Gecz, Jozef
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Schlaeger, Thorsten M.
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Sui, Shannan Ho
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Göke, Jonathan
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Lehtinen, Maria K.
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Pomeroy, Scott L.
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Shi, Yang
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Karwacki-Neisius, Violetta
721c1457-1eb6-4861-8c32-172f91784454
Jang, Ahram
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Cukuroglu, Engin
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Tai, Albert
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Jiao, Alan
c83af8b0-50ec-4228-b068-4555e5558696
Predes, Danilo
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Yoon, Joon
bbb59dd4-dfb9-4ddf-89a0-dd4e2a3d0edd
Brookes, Emily
425dafc2-111b-4f6c-9336-f720c4ef8cac
Chen, Jiekai
bc5d4849-6182-4184-a366-c3db2ae7c1b7
Iberg, Aimee
f7c688df-90d9-4ac7-9f35-12225e8e6983
Halbritter, Florian
fe5272c1-d0b5-4ecf-9a5d-5d6e51f182bd
Õunap, Katrin
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Gecz, Jozef
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Schlaeger, Thorsten M.
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Sui, Shannan Ho
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Göke, Jonathan
a421a9f8-3d2d-49a0-ab8e-bff7fafaf7cc
Lehtinen, Maria K.
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Pomeroy, Scott L.
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Shi, Yang
d52165e4-e3f4-4fe1-97dc-932b4075970b

Karwacki-Neisius, Violetta, Jang, Ahram, Cukuroglu, Engin, Tai, Albert, Jiao, Alan, Predes, Danilo, Yoon, Joon, Brookes, Emily, Chen, Jiekai, Iberg, Aimee, Halbritter, Florian, Õunap, Katrin, Gecz, Jozef, Schlaeger, Thorsten M., Sui, Shannan Ho, Göke, Jonathan, Lehtinen, Maria K., Pomeroy, Scott L. and Shi, Yang (2024) WNT signalling control by KDM5C during development affects cognition. Nature, 627 (8004), 594-603. (doi:10.1038/s41586-024-07067-y).

Record type: Article

Abstract

Although KDM5C is one of the most frequently mutated genes in X-linked intellectual disability1, the exact mechanisms that lead to cognitive impairment remain unknown. Here we use human patient-derived induced pluripotent stem cells and Kdm5c knockout mice to conduct cellular, transcriptomic, chromatin and behavioural studies. KDM5C is identified as a safeguard to ensure that neurodevelopment occurs at an appropriate timescale, the disruption of which leads to intellectual disability. Specifically, there is a developmental window during which KDM5C directly controls WNT output to regulate the timely transition of primary to intermediate progenitor cells and consequently neurogenesis. Treatment with WNT signalling modulators at specific times reveal that only a transient alteration of the canonical WNT signalling pathway is sufficient to rescue the transcriptomic and chromatin landscapes in patient-derived cells and to induce these changes in wild-type cells. Notably, WNT inhibition during this developmental period also rescues behavioural changes of Kdm5c knockout mice. Conversely, a single injection of WNT3A into the brains of wild-type embryonic mice cause anxiety and memory alterations. Our work identifies KDM5C as a crucial sentinel for neurodevelopment and sheds new light on KDM5C mutation-associated intellectual disability. The results also increase our general understanding of memory and anxiety formation, with the identification of WNT functioning in a transient nature to affect long-lasting cognitive function.

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s41586-024-07067-y - Version of Record
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Accepted/In Press date: 12 January 2024
e-pub ahead of print date: 21 February 2024
Published date: 21 March 2024

Identifiers

Local EPrints ID: 490762
URI: http://eprints.soton.ac.uk/id/eprint/490762
ISSN: 0028-0836
PURE UUID: 2797e98f-5d45-4aed-b492-58d64cd72594
ORCID for Emily Brookes: ORCID iD orcid.org/0000-0003-2175-4349

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Date deposited: 06 Jun 2024 16:37
Last modified: 15 Jun 2024 02:06

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Contributors

Author: Violetta Karwacki-Neisius
Author: Ahram Jang
Author: Engin Cukuroglu
Author: Albert Tai
Author: Alan Jiao
Author: Danilo Predes
Author: Joon Yoon
Author: Emily Brookes ORCID iD
Author: Jiekai Chen
Author: Aimee Iberg
Author: Florian Halbritter
Author: Katrin Õunap
Author: Jozef Gecz
Author: Thorsten M. Schlaeger
Author: Shannan Ho Sui
Author: Jonathan Göke
Author: Maria K. Lehtinen
Author: Scott L. Pomeroy
Author: Yang Shi

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