B6.129P2-Sp3^tm1Sus/Cnrm

Status	Available to order
EMMA ID	EM:02429
Citation information	RRID:IMSR_EM:02429 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	B6.129P2-Sp3^tm1Sus/Cnrm
Alternative name	Sp3 knockout
Strain type	Targeted Mutant Strains : Knock-out
Allele/Transgene symbol	Sp3^tm1Sus
Gene/Transgene symbol	Sp3

Information from provider

Provider	Sjaak Philipsen
Provider affiliation	Genetics, Erasmus MC
Genetic information	The targeting vector pBS-P-B-Delta-lacZ-neo-5'-Sp3 was designed to substitute exon 2 (amino acids 38-490) of the mouse Sp3 gene for IRES-LacZ-neo-polyA sequences. The lacZ-neo fusion gene is expressed under the control of the endogenous Sp3 promoter. The deleted sequences encode both glutamine-rich activation domains of Sp3. Thus, the disruption should result in a null allele.
Phenotypic information	Sp3-deficient embryos are growth retarded and invariably die at birth of respiratory failure. Only minor morphological alterations were observed in the lung, and surfactant protein expression is indistinguishable from that of wild-type mice. Histological examinations of individual organs in Sp3-/- mice show a pronounced defect in late tooth formation. In Sp3 null mice, the dentin/enamel layer of the developing teeth is impaired due to the lack of ameloblast-specific gene products. Sp3 is also required for proper skeletal ossification. Both endochondral and intramembranous ossification are impaired in E18.5 Sp3-/- embryos. The absence of Sp3 also results in cell-autonomous hematopoietic defects, affecting in particular the erythroid and myeloid cell lineages. Finally, Sp3 is required for normal cardiac development; this is the likely cause of prenatal death of Sp3-/- embryos in the C57BL/6 background.
Breeding history	The line was backcrossed to C57BL/6 for more than 20 generations.
References	Sp1/Sp3 compound heterozygous mice are not viable: impaired erythropoiesis and severe placental defects.;Krüger Imme, Vollmer Marion, Simmons David G, Elsässer Hans-Peter, Philipsen Sjaak, Suske Guntram, ;2007;Developmental dynamics : an official publication of the American Association of Anatomists;236;2235-44; 17584888 Transcription factor Sp3 knockout mice display serious cardiac malformations.;van Loo Pieter Fokko, Mahtab Edris A F, Wisse Lambertus J, Hou Jun, Grosveld Frank, Suske Guntram, Philipsen Sjaak, Gittenberger-de Groot Adriana C, ;2007;Molecular and cellular biology;27;8571-82; 17923686 Transcription factor Sp3 is essential for post-natal survival and late tooth development.;Bouwman P, Göllner H, Elsässer H P, Eckhoff G, Karis A, Grosveld F, Philipsen S, Suske G, ;2000;The EMBO journal;19;655-61; 10675334 Impaired ossification in mice lacking the transcription factor Sp3.;Göllner H, Dani C, Phillips B, Philipsen S, Suske G, ;2001;Mechanisms of development;106;77-83; 11472836 Impaired hematopoiesis in mice lacking the transcription factor Sp3.;Van Loo Pieter Fokko, Bouwman Peter, Ling Kam-Wing, Middendorp Sabine, Suske Guntram, Grosveld Frank, Dzierzak Elaine, Philipsen Sjaak, Hendriks Rudolf W, ;2003;Blood;102;858-66; 12676787

Information from EMMA

Archiving centre	CNR, Consiglio Nazionale delle Ricerche, Monterotondo, Italy

Disease and phenotype information

MGI phenotypes (allele matching)

decreased body size / MGI
abnormal erythroid progenitor cell morphology / MGI
delayed bone ossification / MGI
abnormal interparietal bone morphology / MGI
abnormal supraoccipital bone morphology / MGI
abnormal nasal bone morphology / MGI
abnormal basisphenoid bone morphology / MGI
abnormal frontal bone morphology / MGI
abnormal parietal bone morphology / MGI
abnormal vertebral body morphology / MGI
abnormal xiphoid process morphology / MGI
abnormal erythropoiesis / MGI
abnormal cranium morphology / MGI
liver hypoplasia / MGI
small thymus / MGI
abnormal placenta labyrinth morphology / MGI
respiratory failure / MGI
abnormal tooth morphology / MGI
abnormal B cell differentiation / MGI
abnormal pulmonary alveolus morphology / MGI
abnormal ameloblast morphology / MGI
abnormal dentin morphology / MGI
abnormal bone mineralization / MGI
abnormal metatarsal bone morphology / MGI
abnormal metacarpal bone morphology / MGI
absent enamel / MGI
delayed endochondral bone ossification / MGI
delayed intramembranous bone ossification / MGI
abnormal sagittal suture morphology / MGI
abnormal presphenoid bone morphology / MGI
abnormal cervical atlas morphology / MGI
abnormal phalanx morphology / MGI
decreased CD4-positive, alpha beta T cell number / MGI
abnormal sternum ossification / MGI
abnormal osteoblast differentiation / MGI
abnormal trophoblast glycogen cell morphology / MGI
abnormal spongiotrophoblast cell morphology / MGI
decreased birth body size / MGI
abnormal basicranium morphology / MGI
neonatal lethality, complete penetrance / MGI
decreased spongiotrophoblast size / MGI

MGI phenotypes (gene matching)

delayed bone ossification / MGI
abnormal interparietal bone morphology / MGI
abnormal supraoccipital bone morphology / MGI
abnormal nasal bone morphology / MGI
abnormal basisphenoid bone morphology / MGI
abnormal frontal bone morphology / MGI
abnormal parietal bone morphology / MGI
abnormal tooth development / MGI
abnormal vertebral body morphology / MGI
abnormal xiphoid process morphology / MGI
abnormal erythropoiesis / MGI
abnormal cranium morphology / MGI
liver hypoplasia / MGI
small thymus / MGI
decreased body size / MGI
abnormal placenta labyrinth morphology / MGI
respiratory failure / MGI
abnormal B cell differentiation / MGI
abnormal pulmonary alveolus morphology / MGI
abnormal ameloblast morphology / MGI
abnormal bone mineralization / MGI
no phenotypic analysis / MGI
abnormal metatarsal bone morphology / MGI
abnormal metacarpal bone morphology / MGI
delayed endochondral bone ossification / MGI
delayed intramembranous bone ossification / MGI
abnormal sagittal suture morphology / MGI
abnormal presphenoid bone morphology / MGI
abnormal cervical atlas morphology / MGI
abnormal phalanx morphology / MGI
decreased CD4-positive, alpha beta T cell number / MGI
abnormal sternum ossification / MGI
abnormal osteoblast differentiation / MGI
abnormal erythroid progenitor cell morphology / MGI
abnormal DNA methylation / MGI
abnormal trophoblast glycogen cell morphology / MGI
abnormal spongiotrophoblast cell morphology / MGI
decreased birth body size / MGI
abnormal basicranium morphology / MGI
neonatal lethality, complete penetrance / MGI
decreased spongiotrophoblast size / MGI
abnormal dentin development / MGI
abnormal enamel development / MGI

Literature references

Sp1/Sp3 compound heterozygous mice are not viable: impaired erythropoiesis and severe placental defects.;Krüger Imme, Vollmer Marion, Simmons David G, Elsässer Hans-Peter, Philipsen Sjaak, Suske Guntram, ;2007;Developmental dynamics : an official publication of the American Association of Anatomists;236;2235-44; 17584888
Transcription factor Sp3 knockout mice display serious cardiac malformations.;van Loo Pieter Fokko, Mahtab Edris A F, Wisse Lambertus J, Hou Jun, Grosveld Frank, Suske Guntram, Philipsen Sjaak, Gittenberger-de Groot Adriana C, ;2007;Molecular and cellular biology;27;8571-82; 17923686
Transcription factor Sp3 is essential for post-natal survival and late tooth development.;Bouwman P, Göllner H, Elsässer H P, Eckhoff G, Karis A, Grosveld F, Philipsen S, Suske G, ;2000;The EMBO journal;19;655-61; 10675334
Impaired ossification in mice lacking the transcription factor Sp3.;Göllner H, Dani C, Phillips B, Philipsen S, Suske G, ;2001;Mechanisms of development;106;77-83; 11472836
Impaired hematopoiesis in mice lacking the transcription factor Sp3.;Van Loo Pieter Fokko, Bouwman Peter, Ling Kam-Wing, Middendorp Sabine, Suske Guntram, Grosveld Frank, Dzierzak Elaine, Philipsen Sjaak, Hendriks Rudolf W, ;2003;Blood;102;858-66; 12676787

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B6.129P2-Sp3tm1Sus/Cnrm