p31 Deficiency Influences Endoplasmic Reticulum Tubular Morphology and Cell Survival

Uemura, Takefumi; Sato, Takashi; Aoki, Takehiro; Yamamoto, Akitsugu; Okada, Tetsuya; Hirai, Rika; Harada, Reiko; Mori, Kazutoshi; Tagaya, Mitsuo; Harada, Akihiro

doi:https://doi.org/10.1128/MCB.01089-08

p31 Deficiency Influences Endoplasmic Reticulum Tubular Morphology and Cell Survival

Uemura, Takefumi; Sato, Takashi; Aoki, Takehiro et al.

Molecular and Cellular Biology, 2009, 29(7), 1869-1881

Number of Access:2,016（2026-02-18 13:15 Counts）

Identifier to cite or link to this item: https://hdl.handle.net/11094/23088

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Title	p31 Deficiency Influences Endoplasmic Reticulum Tubular Morphology and Cell Survival
Creator	NRID 1000080548925 1000080548925 CreatorName Uemura, Takefumi
	NRID 1000040065917 1000040065917 CreatorName Sato, Takashi
	CreatorName Aoki, Takehiro
	NRID 1000030174775 1000030174775 CreatorName Yamamoto, Akitsugu
	NRID 1000070378529 1000070378529 CreatorName Okada, Tetsuya
	CreatorName Hirai, Rika
	NRID 1000040230718 1000040230718 CreatorName Harada, Reiko
	NRID 1000070182194 1000070182194 CreatorName Mori, Kazutoshi
	NRID 1000030179569 1000030179569 CreatorName Tagaya, Mitsuo
	NRID 1000040251441 1000040251441 researchmap permalink aharada aharada Scopus Author ID 7202253419 7202253419 CreatorName Harada, Akihiro
Abstract	p31, the mammalian orthologue of yeast Use1p, is an endoplasmic reticulum (ER)-localized soluble N-ethylmaleimide-sensitive factor attachment protein (SNAP) receptor (SNARE) that forms a complex with other SNAREs, particularly syntaxin 18. However, the role of p31 in ER function remains unknown. To determine the role of p31 in vivo, we generated p31 conditional knockout mice. We found that homozygous deletion of the p31 gene led to early embryonic lethality before embryonic day 8.5. Conditional knockout of p31 in brains and mouse embryonic fibroblasts (MEFs) caused massive apoptosis accompanied by upregulation of ER stress-associated genes. Microscopic analysis showed vesiculation and subsequent enlargement of the ER membrane in p31-deficient cells. This type of drastic disorganization in the ER tubules has not been demonstrated to date. This marked change in ER structure preceded nuclear translocation of the ER stress-related transcription factor C/EBP homologous protein (CHOP), suggesting that ER stress-induced apoptosis resulted from disruption of the ER membrane structure. Taken together, these results suggest that p31 is an essential molecule involved in the maintenance of ER morphology and that its deficiency leads to ER stress-induced apoptosis.
Publisher	American Society for Microbiology
Source Title	Molecular and Cellular Biology
Volume (Issue)	29(7)
Page	1869-1881
Date of Issued	2009-04
Language	English
Handle URL	https://hdl.handle.net/11094/23088
PISSN	02707306
NCID	AA10620925
Relation.isIdenticalTo	DOI (Publisher Version) https://doi.org/10.1128/MCB.01089-08
Access Rights	open access
oaire:version	Version of Record
Category	学術雑誌論文 Journal Article

Resource Type	journal article
Local Type	Journal Article
DCMI Type	Text
DCTERMS.bibliographicCitation	Molecular and Cellular Biology. 2009, 29(7), p. 1869-1881
DC.title	p31 Deficiency Influences Endoplasmic Reticulum Tubular Morphology and Cell Survival
DC.creator	Uemura, Takefumi
	Sato, Takashi
	Aoki, Takehiro
	Yamamoto, Akitsugu
	Okada, Tetsuya
	Hirai, Rika
	Harada, Reiko
	Mori, Kazutoshi
	Tagaya, Mitsuo
	Harada, Akihiro
DC.publisher	American Society for Microbiology
DC.language' scheme='DCTERMS.RFC1766	English
DC.type' scheme='DCTERMS.DCMIType	Text
DCTERMS.issued' scheme='DCTERMS.W3CDTF	2009-04
DC.identifier	https://doi.org/10.1128/MCB.01089-08
DCTERMS.abstract	p31, the mammalian orthologue of yeast Use1p, is an endoplasmic reticulum (ER)-localized soluble N-ethylmaleimide-sensitive factor attachment protein (SNAP) receptor (SNARE) that forms a complex with other SNAREs, particularly syntaxin 18. However, the role of p31 in ER function remains unknown. To determine the role of p31 in vivo, we generated p31 conditional knockout mice. We found that homozygous deletion of the p31 gene led to early embryonic lethality before embryonic day 8.5. Conditional knockout of p31 in brains and mouse embryonic fibroblasts (MEFs) caused massive apoptosis accompanied by upregulation of ER stress-associated genes. Microscopic analysis showed vesiculation and subsequent enlargement of the ER membrane in p31-deficient cells. This type of drastic disorganization in the ER tubules has not been demonstrated to date. This marked change in ER structure preceded nuclear translocation of the ER stress-related transcription factor C/EBP homologous protein (CHOP), suggesting that ER stress-induced apoptosis resulted from disruption of the ER membrane structure. Taken together, these results suggest that p31 is an essential molecule involved in the maintenance of ER morphology and that its deficiency leads to ER stress-induced apoptosis.
DC.format	23088
citation_title	p31 Deficiency Influences Endoplasmic Reticulum Tubular Morphology and Cell Survival
citation_author	Uemura, Takefumi
	Sato, Takashi
	Aoki, Takehiro
	Yamamoto, Akitsugu
	Okada, Tetsuya
	Hirai, Rika
	Harada, Reiko
	Mori, Kazutoshi
	Tagaya, Mitsuo
	Harada, Akihiro
citation_publisher	American Society for Microbiology
citation_language	English
citation_date	2009-04
citation_journal_title	Molecular and Cellular Biology
citation_volume	29
citation_issue	7
citation_firstpage	1869
citation_lastpage	1881
citation_doi	https://doi.org/10.1128/MCB.01089-08
citation_public_url	https://hdl.handle.net/11094/23088

p31 Deficiency Influences Endoplasmic Reticulum Tubular Morphology and Cell Survival

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