Delayed Development of Nervous System in Mice Homozygous for Disrupted Microtubule-associated Protein 1B (MAP1B) Gene

Takei, Yosuke; Kondo, Satoru; Harada, Akihiro; Inomata, Satomi; Noda, Tetsuo; Hirokawa, Nobutaka

doi:info:doi/10.1083/jcb.137.7.1615

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タイトル	Delayed Development of Nervous System in Mice Homozygous for Disrupted Microtubule-associated Protein 1B (MAP1B) Gene
著者	Takei, Yosuke Takei, Yosuke
	Kondo, Satoru Kondo, Satoru
	Harada, Akihiro Harada, Akihiro
	Inomata, Satomi Inomata, Satomi
	Noda, Tetsuo Noda, Tetsuo
	Hirokawa, Nobutaka Hirokawa, Nobutaka
抄録	Microtubule-associated protein 1B (MAP1B), one of the microtubule-associated proteins (MAPs), is a major component of the neuronal cytoskeleton. It is expressed at high levels in immature neurons during growth of their axons, which indicates that it plays a crucial role in neuronal morphogenesis and neurite extension. To better define the role of MAP1B in vivo, we have used gene targeting to disrupt the murine MAP1B gene. Heterozygotes of our MAP1B disruption exhibit no overt abnormalities in their development and behavior, while homozygotes showed a slightly decreased brain weight and delayed nervous system development. Our data indicate that while MAP1B is not essential for survival, it is essential for normal time course development of the murine nervous system. These conclusions are very different from those of a previous MAP1B gene–targeting study (Edelmann, W., M. Zervas, P. Costello, L. Roback, I. Fischer, A. Hammarback, N. Cowan, P. Davis, B. Wainer, and R. Kucherlapati. 1996. Proc. Natl. Acad. Sci. USA. 93: 1270–1275). In this previous effort, homozygotes died before reaching 8-d embryos, while heterozygotes showed severely abnormal phenotypes in their nervous systems. Because the gene targeting event in these mice produced a gene encoding a 571–amino acid truncated product of MAP1B, it seems likely that the phenotypes seen arise from the truncated MAP1B product acting in a dominant-negative fashion, rather than a loss of MAP1B function.
公開者	The Rockefeller University Press
掲載誌名	Journal of Cell Biology
巻	137
号	7
開始ページ	1615
終了ページ	1626
刊行年月	1997-06-30
ISSN	00219525
NCID	AA00694812
DOI	info:doi/10.1083/jcb.137.7.1615
URL	http://hdl.handle.net/11094/23091
言語	英語
カテゴリ	学術雑誌論文 Journal Article

著者版フラグ	publisher
NII資源タイプ	学術雑誌論文
ローカル資源タイプ	学術雑誌論文
dcmi資源タイプ	text
DCTERMS.bibliographicCitation	Journal of Cell Biology.137(7) P.1615-P.1626
DC.title	Delayed Development of Nervous System in Mice Homozygous for Disrupted Microtubule-associated Protein 1B (MAP1B) Gene
DC.creator	Takei, Yosuke
	Kondo, Satoru
	Harada, Akihiro
	Inomata, Satomi
	Noda, Tetsuo
	Hirokawa, Nobutaka
DC.publisher	The Rockefeller University Press
DC.language" scheme="DCTERMS.RFC1766	英語
DCTERMS.issued" scheme="DCTERMS.W3CDTF	1997-06-30
DC.identifier	info:doi/10.1083/jcb.137.7.1615
DC.identifier" scheme="DCTERMS.URI	http://hdl.handle.net/11094/23091
DCTERMS.abstract	Microtubule-associated protein 1B (MAP1B), one of the microtubule-associated proteins (MAPs), is a major component of the neuronal cytoskeleton. It is expressed at high levels in immature neurons during growth of their axons, which indicates that it plays a crucial role in neuronal morphogenesis and neurite extension. To better define the role of MAP1B in vivo, we have used gene targeting to disrupt the murine MAP1B gene. Heterozygotes of our MAP1B disruption exhibit no overt abnormalities in their development and behavior, while homozygotes showed a slightly decreased brain weight and delayed nervous system development. Our data indicate that while MAP1B is not essential for survival, it is essential for normal time course development of the murine nervous system. These conclusions are very different from those of a previous MAP1B gene–targeting study (Edelmann, W., M. Zervas, P. Costello, L. Roback, I. Fischer, A. Hammarback, N. Cowan, P. Davis, B. Wainer, and R. Kucherlapati. 1996. Proc. Natl. Acad. Sci. USA. 93: 1270–1275). In this previous effort, homozygotes died before reaching 8-d embryos, while heterozygotes showed severely abnormal phenotypes in their nervous systems. Because the gene targeting event in these mice produced a gene encoding a 571–amino acid truncated product of MAP1B, it seems likely that the phenotypes seen arise from the truncated MAP1B product acting in a dominant-negative fashion, rather than a loss of MAP1B function.
citation_title	Delayed Development of Nervous System in Mice Homozygous for Disrupted Microtubule-associated Protein 1B (MAP1B) Gene
citation_author	Takei, Yosuke
	Kondo, Satoru
	Harada, Akihiro
	Inomata, Satomi
	Noda, Tetsuo
	Hirokawa, Nobutaka
citation_publisher	The Rockefeller University Press
citation_language	英語
citation_date	1997-06-30
citation_journal_title	Journal of Cell Biology
citation_volume	137
citation_issue	7
citation_firstpage	1615
citation_lastpage	1626
citation_issn	00219525
citation_doi	info:doi/10.1083/jcb.137.7.1615
citation_public_url	http://hdl.handle.net/11094/23091

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