The psychiatric disease risk factors DISC1 and TNIK interact to regulate synapse composition and function

Q. Wang; E. I. Charych; V. L. Pulito; J. B. Lee; N. M. Graziane; R. A. Crozier; R. Revilla-Sanchez; M. P. Kelly; A. J. Dunlop; H. Murdoch; N. Taylor; Y. Xie; M. Pausch; A. Hayashi-Takagi; K. Ishizuka; S. Seshadri; B. Bates; K. Kariya; A. Sawa; R. J. Weinberg; S. J. Moss; M. D. Houslay; Z. Yan; N. J. Brandon

doi:10.1038/mp.2010.87

The psychiatric disease risk factors DISC1 and TNIK interact to regulate synapse composition and function

Q. Wang, E. I. Charych, V. L. Pulito, J. B. Lee, N. M. Graziane, R. A. Crozier, R. Revilla-Sanchez, M. P. Kelly, A. J. Dunlop, H. Murdoch, N. Taylor, Y. Xie, M. Pausch, A. Hayashi-Takagi, K. Ishizuka, S. Seshadri, B. Bates, K. Kariya, A. Sawa, R. J. WeinbergS. J. Moss, M. D. Houslay, Z. Yan, N. J. Brandon

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Abstract

Disrupted in schizophrenia 1 (DISC1), a genetic risk factor for multiple serious psychiatric diseases including schizophrenia, bipolar disorder and autism, is a key regulator of multiple neuronal functions linked to both normal development and disease processes. As these diseases are thought to share a common deficit in synaptic function and architecture, we have analyzed the role of DISC1 using an approach that focuses on understanding the protein-protein interactions of DISC1 specifically at synapses. We identify the Traf2 and Nck-interacting kinase (TNIK), an emerging risk factor itself for disease, as a key synaptic partner for DISC1, and provide evidence that the DISC1-TNIK interaction regulates synaptic composition and activity by stabilizing the levels of key postsynaptic density proteins. Understanding the novel DISC1-TNIK interaction is likely to provide insights into the etiology and underlying synaptic deficits found in major psychiatric diseases.

Original language	English (US)
Pages (from-to)	1006-1023
Number of pages	18
Journal	Molecular Psychiatry
Volume	16
Issue number	10
DOIs	https://doi.org/10.1038/mp.2010.87
State	Published - Oct 2011

All Science Journal Classification (ASJC) codes

Molecular Biology
Cellular and Molecular Neuroscience
Psychiatry and Mental health

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10.1038/mp.2010.87

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Wang, Q., Charych, E. I., Pulito, V. L., Lee, J. B., Graziane, N. M., Crozier, R. A., Revilla-Sanchez, R., Kelly, M. P., Dunlop, A. J., Murdoch, H., Taylor, N., Xie, Y., Pausch, M., Hayashi-Takagi, A., Ishizuka, K., Seshadri, S., Bates, B., Kariya, K., Sawa, A., ... Brandon, N. J. (2011). The psychiatric disease risk factors DISC1 and TNIK interact to regulate synapse composition and function. Molecular Psychiatry, 16(10), 1006-1023. https://doi.org/10.1038/mp.2010.87

@article{af94f06fcc01451990d278739efa172f,

title = "The psychiatric disease risk factors DISC1 and TNIK interact to regulate synapse composition and function",

abstract = "Disrupted in schizophrenia 1 (DISC1), a genetic risk factor for multiple serious psychiatric diseases including schizophrenia, bipolar disorder and autism, is a key regulator of multiple neuronal functions linked to both normal development and disease processes. As these diseases are thought to share a common deficit in synaptic function and architecture, we have analyzed the role of DISC1 using an approach that focuses on understanding the protein-protein interactions of DISC1 specifically at synapses. We identify the Traf2 and Nck-interacting kinase (TNIK), an emerging risk factor itself for disease, as a key synaptic partner for DISC1, and provide evidence that the DISC1-TNIK interaction regulates synaptic composition and activity by stabilizing the levels of key postsynaptic density proteins. Understanding the novel DISC1-TNIK interaction is likely to provide insights into the etiology and underlying synaptic deficits found in major psychiatric diseases.",

author = "Q. Wang and Charych, {E. I.} and Pulito, {V. L.} and Lee, {J. B.} and Graziane, {N. M.} and Crozier, {R. A.} and R. Revilla-Sanchez and Kelly, {M. P.} and Dunlop, {A. J.} and H. Murdoch and N. Taylor and Y. Xie and M. Pausch and A. Hayashi-Takagi and K. Ishizuka and S. Seshadri and B. Bates and K. Kariya and A. Sawa and Weinberg, {R. J.} and Moss, {S. J.} and Houslay, {M. D.} and Z. Yan and Brandon, {N. J.}",

year = "2011",

month = oct,

doi = "10.1038/mp.2010.87",

language = "English (US)",

volume = "16",

pages = "1006--1023",

journal = "Molecular Psychiatry",

issn = "1359-4184",

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Wang, Q, Charych, EI, Pulito, VL, Lee, JB, Graziane, NM, Crozier, RA, Revilla-Sanchez, R, Kelly, MP, Dunlop, AJ, Murdoch, H, Taylor, N, Xie, Y, Pausch, M, Hayashi-Takagi, A, Ishizuka, K, Seshadri, S, Bates, B, Kariya, K, Sawa, A, Weinberg, RJ, Moss, SJ, Houslay, MD, Yan, Z & Brandon, NJ 2011, 'The psychiatric disease risk factors DISC1 and TNIK interact to regulate synapse composition and function', Molecular Psychiatry, vol. 16, no. 10, pp. 1006-1023. https://doi.org/10.1038/mp.2010.87

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AU - Wang, Q.

AU - Charych, E. I.

AU - Pulito, V. L.

AU - Lee, J. B.

AU - Graziane, N. M.

AU - Crozier, R. A.

AU - Revilla-Sanchez, R.

AU - Kelly, M. P.

AU - Dunlop, A. J.

AU - Murdoch, H.

AU - Taylor, N.

AU - Xie, Y.

AU - Pausch, M.

AU - Hayashi-Takagi, A.

AU - Ishizuka, K.

AU - Seshadri, S.

AU - Bates, B.

AU - Kariya, K.

AU - Sawa, A.

AU - Weinberg, R. J.

AU - Moss, S. J.

AU - Houslay, M. D.

AU - Yan, Z.

AU - Brandon, N. J.

PY - 2011/10

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AB - Disrupted in schizophrenia 1 (DISC1), a genetic risk factor for multiple serious psychiatric diseases including schizophrenia, bipolar disorder and autism, is a key regulator of multiple neuronal functions linked to both normal development and disease processes. As these diseases are thought to share a common deficit in synaptic function and architecture, we have analyzed the role of DISC1 using an approach that focuses on understanding the protein-protein interactions of DISC1 specifically at synapses. We identify the Traf2 and Nck-interacting kinase (TNIK), an emerging risk factor itself for disease, as a key synaptic partner for DISC1, and provide evidence that the DISC1-TNIK interaction regulates synaptic composition and activity by stabilizing the levels of key postsynaptic density proteins. Understanding the novel DISC1-TNIK interaction is likely to provide insights into the etiology and underlying synaptic deficits found in major psychiatric diseases.

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The psychiatric disease risk factors DISC1 and TNIK interact to regulate synapse composition and function

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