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Article: Null Mutation of the Lmo4 Gene or a Combined Null Mutation of the Lmo1/ Lmo3 Genes Causes Perinatal Lethality, and Lmo4 Controls Neural Tube Development in Mice

TitleNull Mutation of the Lmo4 Gene or a Combined Null Mutation of the Lmo1/ Lmo3 Genes Causes Perinatal Lethality, and Lmo4 Controls Neural Tube Development in Mice
Authors
Issue Date2004
Citation
Molecular And Cellular Biology, 2004, v. 24 n. 5, p. 2063-2073 How to Cite?
AbstractThe LIM-only family of proteins comprises four members; two of these (LMO1 and LMO2) are involved in human T-cell leukemia via chromosomal translocations, and LMO2 is a master regulator of hematopoiesis. We have carried out gene targeting of the other members of the LIM-only family, viz., genes Lmo1, Lmo3 and Lmo4, to investigate their role in mouse development. None of these genes has an obligatory role in lymphopoiesis. In addition, while null mutations of Lmo1 or Lmo3 have no discernible phenotype, null mutation of Lmo4 alone causes perinatal lethality due to a severe neural tube defect which occurs in the form of anencephaly or exencephaly. Since the Lmo1 and Lmo3 gene sequences are highly related and have partly overlapping expression domains, we assessed the effect of compound Lmo1/Lmo3 null mutations. Although no anatomical defects were apparent in compound null pups, these animals also die within 24 h of birth, suggesting that a compensation between the related Lmo1 and 3 proteins can occur during embryogenesis to negate the individual loss of these genes. Our results complete the gene targeting of the LIM-only family in mice and suggest that all four members of this family are important in regulators of distinct developmental pathways.
Persistent Identifierhttp://hdl.handle.net/10722/162768
ISSN
2015 Impact Factor: 4.427
2015 SCImago Journal Rankings: 3.806
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorTse, Een_US
dc.contributor.authorSmith, AJHen_US
dc.contributor.authorHunt, Sen_US
dc.contributor.authorLavenir, Ien_US
dc.contributor.authorForster, Aen_US
dc.contributor.authorWarren, AJen_US
dc.contributor.authorGrutz, Gen_US
dc.contributor.authorForoni, Len_US
dc.contributor.authorCarlton, MBLen_US
dc.contributor.authorColledge, WHen_US
dc.contributor.authorBoehm, Ten_US
dc.contributor.authorRabbitts, THen_US
dc.date.accessioned2012-09-05T05:23:16Z-
dc.date.available2012-09-05T05:23:16Z-
dc.date.issued2004en_US
dc.identifier.citationMolecular And Cellular Biology, 2004, v. 24 n. 5, p. 2063-2073en_US
dc.identifier.issn0270-7306en_US
dc.identifier.urihttp://hdl.handle.net/10722/162768-
dc.description.abstractThe LIM-only family of proteins comprises four members; two of these (LMO1 and LMO2) are involved in human T-cell leukemia via chromosomal translocations, and LMO2 is a master regulator of hematopoiesis. We have carried out gene targeting of the other members of the LIM-only family, viz., genes Lmo1, Lmo3 and Lmo4, to investigate their role in mouse development. None of these genes has an obligatory role in lymphopoiesis. In addition, while null mutations of Lmo1 or Lmo3 have no discernible phenotype, null mutation of Lmo4 alone causes perinatal lethality due to a severe neural tube defect which occurs in the form of anencephaly or exencephaly. Since the Lmo1 and Lmo3 gene sequences are highly related and have partly overlapping expression domains, we assessed the effect of compound Lmo1/Lmo3 null mutations. Although no anatomical defects were apparent in compound null pups, these animals also die within 24 h of birth, suggesting that a compensation between the related Lmo1 and 3 proteins can occur during embryogenesis to negate the individual loss of these genes. Our results complete the gene targeting of the LIM-only family in mice and suggest that all four members of this family are important in regulators of distinct developmental pathways.en_US
dc.languageengen_US
dc.relation.ispartofMolecular and Cellular Biologyen_US
dc.subject.meshAdaptor Proteins, Signal Transducingen_US
dc.subject.meshAmino Acid Sequenceen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAnimals, Newbornen_US
dc.subject.meshCentral Nervous System - Embryology - Pathology - Physiologyen_US
dc.subject.meshDna-Binding Proteins - Genetics - Metabolismen_US
dc.subject.meshEmbryonic And Fetal Developmenten_US
dc.subject.meshFemaleen_US
dc.subject.meshGene Targetingen_US
dc.subject.meshGenotypeen_US
dc.subject.meshHomeodomain Proteins - Genetics - Metabolismen_US
dc.subject.meshHumansen_US
dc.subject.meshLim Domain Proteinsen_US
dc.subject.meshMaleen_US
dc.subject.meshMiceen_US
dc.subject.meshMice, Inbred C57blen_US
dc.subject.meshMolecular Sequence Dataen_US
dc.subject.meshMorphogenesisen_US
dc.subject.meshMutationen_US
dc.subject.meshOncogene Proteins - Genetics - Metabolismen_US
dc.subject.meshSequence Alignmenten_US
dc.subject.meshTranscription Factors - Genetics - Metabolismen_US
dc.titleNull Mutation of the Lmo4 Gene or a Combined Null Mutation of the Lmo1/ Lmo3 Genes Causes Perinatal Lethality, and Lmo4 Controls Neural Tube Development in Miceen_US
dc.typeArticleen_US
dc.identifier.emailTse, E:ewctse@hku.hken_US
dc.identifier.authorityTse, E=rp00471en_US
dc.description.naturelink_to_OA_fulltexten_US
dc.identifier.doi10.1128/MCB.24.5.2063-2073.2004en_US
dc.identifier.pmid14966285-
dc.identifier.scopuseid_2-s2.0-10744229888en_US
dc.identifier.hkuros87911-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-10744229888&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume24en_US
dc.identifier.issue5en_US
dc.identifier.spage2063en_US
dc.identifier.epage2073en_US
dc.identifier.isiWOS:000189309500021-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridTse, E=7005019454en_US
dc.identifier.scopusauthoridSmith, AJH=7406757495en_US
dc.identifier.scopusauthoridHunt, S=7402383409en_US
dc.identifier.scopusauthoridLavenir, I=6602741549en_US
dc.identifier.scopusauthoridForster, A=7201638425en_US
dc.identifier.scopusauthoridWarren, AJ=16737062300en_US
dc.identifier.scopusauthoridGrutz, G=14524658600en_US
dc.identifier.scopusauthoridForoni, L=7005279817en_US
dc.identifier.scopusauthoridCarlton, MBL=35515164600en_US
dc.identifier.scopusauthoridColledge, WH=7006668544en_US
dc.identifier.scopusauthoridBoehm, T=7103237660en_US
dc.identifier.scopusauthoridRabbitts, TH=7103136845en_US

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