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  1. F100 環境医学研究所
  2. F100a 雑誌掲載論文
  3. 学術雑誌

Myosin Va mutation in rats is an animal model for the human hereditary neurological disease, Griscelli syndrome type 1

http://hdl.handle.net/2237/10947
http://hdl.handle.net/2237/10947
d2621236-af96-4ba7-9409-ee5ff2c957a2
名前 / ファイル ライセンス アクション
Takagishi_Murata_plus_Figs.pdf Takagishi_Murata_plus_Figs.pdf (16.2 MB)
Item type 学術雑誌論文 / Journal Article(1)
公開日 2009-01-27
タイトル
タイトル Myosin Va mutation in rats is an animal model for the human hereditary neurological disease, Griscelli syndrome type 1
言語 en
著者 Takagishi, Yoshiko

× Takagishi, Yoshiko

WEKO 25817

en Takagishi, Yoshiko

Search repository
高岸, 芳子

× 高岸, 芳子

WEKO 25818

ja 高岸, 芳子

Search repository
Murata, Yoshiharu

× Murata, Yoshiharu

WEKO 25819

en Murata, Yoshiharu

Search repository
アクセス権
アクセス権 open access
アクセス権URI http://purl.org/coar/access_right/c_abf2
キーワード
主題Scheme Other
主題 mutant
キーワード
主題Scheme Other
主題 cerebellum
キーワード
主題Scheme Other
主題 smooth endoplasmic reticulum
キーワード
主題Scheme Other
主題 Purkinje cells
キーワード
主題Scheme Other
主題 calcium
キーワード
主題Scheme Other
主題 synaptic plasticity
抄録
内容記述 A spontaneous neurological mutation, dilute-opisthotonus (dop), was discovered in our breeding colony of Wistar rats. We found that the mutation affected the gene encoding Myosin Va (MyoVA), an actin-based molecular motor. Analysis of the myosin Va (Myo5a) gene of the dop genome showed the presence of a complex rearrangement consisting of a 306-bp inversion associated with 217-bp and 17-bp deletions. A 141 bp exon is skipped in the dop transcript, producing a dop cDNA with a 141 in-frame deletion in the sequences encoding the head region. Expression of the MyoVA protein is severely impaired in the brains of dop homozygous rats, suggesting they have a null mutation for Myo5a. In a morphological analysis of the cerebella of dop rats, we found an absence of smooth endoplasmic reticulum (SER) and of inositol 1,4,5-triphosphate (IP3) receptors in the dendritic spines of Purkinje cells (PC). The SER acts as an intracellular Ca2+ store and IP3-mediated Ca2+ signaling in dendritic spines plays a critical role in synaptic regulation. We therefore measured synaptic transmission and long-term depression (LTD), a form of synaptic plasticity underlying cerebellar motor learning, at PC synapses in the cerebella of dop rats. We found that synaptic transmission at the PC synapses is largely normal, while the LTD is deficient due to a decrease in IP3-mediated Ca2+ release from the SER in the PC spines of the dop cerebella. These findings may account for the ataxic movements and clonic convulsions displayed by dop rats. They also contribute to our understanding of the neurological disease mechanisms of the human hereditary disease Griscelli syndrome type 1, which is caused by mutation of the MYO5A gene.
言語 en
内容記述タイプ Abstract
出版者
言語 en
出版者 New York Academy of Sciences
言語
言語 eng
資源タイプ
資源タイプresource http://purl.org/coar/resource_type/c_6501
タイプ journal article
出版タイプ
出版タイプ AM
出版タイプResource http://purl.org/coar/version/c_ab4af688f83e57aa
DOI
関連タイプ isVersionOf
識別子タイプ DOI
関連識別子 https://doi.org/10.1196/annals.1377.006
ISSN
収録物識別子タイプ PISSN
収録物識別子 00778923
書誌情報 en : Annals of the New York Academy of Sciences

巻 1086, p. 66-80, 発行日 2006-11
フォーマット
application/pdf
著者版フラグ
値 author
URI
識別子 http://hdl.handle.net/2237/10947
識別子タイプ HDL
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