B6;129S-Flrt3^tm1Rob/RobH

Status	Available to order
EMMA ID	EM:08316
Citation information	RRID:IMSR_EM:08316 Research Resource Identifiers (RRID) are persistent unique ID numbers assigned to help researchers cite key resources (e.g. antibodies, model organisms and software projects) in the biomedical literature to improve transparency and reproducibility in research. See https://www.rrids.org/ for more information.
International strain name	B6;129S-Flrt3^tm1Rob/RobH
Alternative name	Flrt3 tm1Rob
Strain type	Targeted Mutant Strains : Knock-out
Allele/Transgene symbol	Flrt3^tm1Rob
Gene/Transgene symbol	Flrt3

Information from provider

Provider	Elizabeth Robertson
Provider affiliation	Sir William Dunn School of Pathology, University of Oxford
Genetic information	Insertion of a beta-geo STOP polyA cassette upstream of Flrt3 exon 3. This generated a null allele as assessed by lack of Flrt3 protein.
Phenotypic information	Homozygous: Mouse embryos deficient in Flrt3 display defects in headfold fusion, definitive endoderm migration and a failure of the lateral edges of the ventral body wall to fuse, leading to cardia bifida. A small proportion of homozygous mutants survives gestation and develops as viable fertile animals (less than 3%). Heterozygous: Heterozygous mice have no phenotype.
Breeding history	Strain is currently maintained on C57BL/6J as heterozygous crosses.
References	Ventral closure, headfold fusion and definitive endoderm migration defects in mouse embryos lacking the fibronectin leucine-rich transmembrane protein FLRT3.;Maretto Silvia, Müller Pari-Sima, Aricescu A Radu, Cho Ken W Y, Bikoff Elizabeth K, Robertson Elizabeth J, ;2008;Developmental biology;318;184-93; 18448090
Homozygous fertile	yes
Homozygous viable	no
Homozygous matings required	no
Immunocompromised	no

Information from EMMA

Archiving centre	Mary Lyon Centre at MRC Harwell, Oxford, United Kingdom

Disease and phenotype information

Orphanet associated rare diseases, based on orthologous gene matching

Kallmann syndrome / Orphanet_478

MGI phenotypes (allele matching)

impaired basement membrane formation / MGI
preweaning lethality, incomplete penetrance / MGI
abnormal heart development / MGI
incomplete rostral neuropore closure / MGI
abnormal endoderm development / MGI
abnormal embryonic tissue morphology / MGI
abnormal neural tube closure / MGI
cardia bifida / MGI
abnormal embryonic neuroepithelium morphology / MGI
embryonic lethality during organogenesis, incomplete penetrance / MGI
rostral body truncation / MGI
failure of ventral body wall closure / MGI

MGI phenotypes (gene matching)

abnormal heart development / MGI
incomplete rostral neuropore closure / MGI
abnormal embryo development / MGI
abnormal endoderm development / MGI
abnormal embryonic tissue morphology / MGI
abnormal neural tube morphology / MGI
impaired basement membrane formation / MGI
abnormal neural tube closure / MGI
embryonic growth retardation / MGI
disorganized embryonic tissue / MGI
failure of initiation of embryo turning / MGI
cardia bifida / MGI
abnormal embryonic neuroepithelium morphology / MGI
abnormal basement membrane morphology / MGI
abnormal anterior visceral endoderm morphology / MGI
postnatal lethality, incomplete penetrance / MGI
embryonic lethality during organogenesis, incomplete penetrance / MGI
preweaning lethality, incomplete penetrance / MGI
rostral body truncation / MGI
failure of ventral body wall closure / MGI

Literature references

Ventral closure, headfold fusion and definitive endoderm migration defects in mouse embryos lacking the fibronectin leucine-rich transmembrane protein FLRT3.;Maretto Silvia, Müller Pari-Sima, Aricescu A Radu, Cho Ken W Y, Bikoff Elizabeth K, Robertson Elizabeth J, ;2008;Developmental biology;318;184-93; 18448090

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B6;129S-Flrt3tm1Rob/RobH