title: Expression analysis of actin-related genes as an underlying mechanism for mood disorders.
abstract: In this study, we explored the newly postulated 'disturbed cytoskeletal' theory of mood disorders. Firstly, we identified Cap1, a gene for important mediator of actin turnover, as a cogent quantitative trait gene for depressive trait of mice by combining the results of our prior genetic and current genome-wide expression analyses. Then we rigorously examined 'core' actin-related gene expression in the frontal cortex of C57BL/6 (B6) (prone to depression) and C3H/He (C3) (resistant to depression) mice. We confirmed that Cap1 was down-regulated at both transcript and protein levels in B6. Other differentially regulated genes included cofilin1 and profilin1 (up-regulated in B6), and a Rho-family GTPase member (Pak1) (down-regulated in B6). Thirdly, we investigated the 'core' actin-pathway components in human postmortem prefrontal cortices, and observed trend for CAP1 reduction in the bipolar brains. These data suggest that the balance of actin dynamics might be altered towards actin depolymerization in mood disorders.
authors.affiliation: Laboratory for Molecular Psychiatry, RIKEN Brain Science Institute, Saitama, Japan.
authors.forename: Noriaki
authors.initials: N
authors.lastname: Nakatani
authors.forename: Tetsuo
authors.initials: T
authors.lastname: Ohnishi
authors.forename: Kazuya
authors.initials: K
authors.lastname: Iwamoto
authors.forename: Akiko
authors.initials: A
authors.lastname: Watanabe
authors.forename: Yoshimi
authors.initials: Y
authors.lastname: Iwayama
authors.forename: Shunji
authors.initials: S
authors.lastname: Yamashita
authors.forename: Yuichi
authors.initials: Y
authors.lastname: Ishitsuka
authors.forename: Kenji
authors.initials: K
authors.lastname: Moriyama
authors.forename: Mizuho
authors.initials: M
authors.lastname: Nakajima
authors.forename: Yoshitaka
authors.initials: Y
authors.lastname: Tatebayashi
authors.forename: Haruhiko
authors.initials: H
authors.lastname: Akiyama
authors.forename: Teruhiko
authors.initials: T
authors.lastname: Higuchi
authors.forename: Tadafumi
authors.initials: T
authors.lastname: Kato
authors.forename: Takeo
authors.initials: T
authors.lastname: Yoshikawa
mesh_terms: D000199:Actins / Q000235:genetics / Q000378:metabolism*; D000818:Animals; D018797:Cell Cycle Proteins / Q000235:genetics / Q000378:metabolism*; D051338:Cofilin 1 / Q000378:metabolism*; D003598:Cytoskeletal Proteins / Q000235:genetics / Q000378:metabolism*; D005625:Frontal Lobe / Q000378:metabolism*; D020869:Gene Expression Profiling; D020022:Genetic Predisposition to Disease / Q000235:genetics; D006801:Humans; D051379:Mice; D019964:Mood Disorders / Q000235:genetics / Q000378:metabolism*; D051304:Profilins / Q000378:metabolism*; D017346:Protein Serine-Threonine Kinases / Q000378:metabolism*; D013045:Species Specificity; D054462:p21-Activated Kinases
chemical_list: D000199:Actins; C489549:CAP1 protein, human; D018797:Cell Cycle Proteins; D051338:Cofilin 1; D003598:Cytoskeletal Proteins; C495738:PFN1 protein, human; D051304:Profilins; C515903:PAK1 protein, human; C515905:Pak1 protein, mouse; D017346:Protein Serine-Threonine Kinases; D054462:p21-Activated Kinases