IMPC phenotypes (gene matching)
- anophthalmia / IMPC
CD1;129-Ibsptm1Jeau Spp1em1Jeau/Orl
| Status | Available to order |
| EMMA ID | EM:15971 |
| Citation information | RRID:IMSR_EM:15971 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 | CD1;129-Ibsptm1Jeau Spp1em1Jeau/Orl |
| Alternative name | BSP and osteopontin double knockout, Ibsp-/- Spp1-/- (Mut15) |
| Strain type | Targeted Mutant Strains : Knock-out |
| Allele/Transgene symbol | Ibsptm1Jeau, Spp1em1Jeau |
| Gene/Transgene symbol | Ibsp, Spp1 |
Information from provider
| Provider | Luc Malaval |
| Provider affiliation | U1059-SAINBIOSE, INSERM |
| Additional owner | Dr Jane E Aubin, Professor Emerita, University of Toronto. Canada. |
| Genetic information | In this mouse line both the Ibsp gene, coding of bone sialoprotein, and the Spp1 gene, coding for osteopontin, have been knocked-out (Bouleftour W et al., Bone, 2019, 120:411-422). |
| Phenotypic information | Homozygous:Ibsp-/- Spp1-/- mice are viable and breed normally, but their weight and size are lower than wild-type mice. They display a lower mineral density than wild-type, with high macroporosity of cortical long bones. The trabecular bone volume is lower at 2 months that in wild-type, with high bone formation and bone resorption rates (Bouleftour W et al., Bone, 2019, 120 :411-422; Malaval L et al., Calcified Tissue International, 2024, 115(1):63-77).Heterozygous:The phenotype of heterozygous mice is indistinguable from that of wild-type mice of same genetic background. |
| Breeding history | We used a targeted mutation approach in Ibsp-/- mice previously generated through homologous recombination (this line is described, see EMMA strain EM:15962). We designed two pairs of TALE nuclease subunits (TALEN) targeting Spp1 exon 5, and checked that, after transfection of the TALEN expression plasmids in mouse MEF cells, they were able to generate targeted mutations in Spp1 exon 5 by the T7E1 assay. In the Plateau de Biologie Expérimentale de la Souris (PBES, ENS, Lyon, France) wild-type CD1 oocytes were fertilized in vitro with sperm taken from Ibsp-/- male mice. The heterozygous eggs were microinjected with the TALEN subunits mRNAs, then implanted in pseudo-pregnant females. Mice from the first (G1) and subsequent generations were screened for Spp1 gene mutations by PCR amplification and sequencing (Eurofins Genomics, Ebersberg, Germany) of the target site in DNA from clipped tail samples. G1 mice were crossed with wild-type 129Sv/CD1 mice and the descent interbred in order to obtain homozygous single Spp1 knock-out mice (Ibsp+/+ Spp1-/-, Mut 1) and double knock-out mice (Ibsp-/- Spp1-/-, Mut15; this strain), which are concerned with the present submission. The procedure is described in detail in Bouleftour W et al., Bone, 2019, 120 :411-422. The Spp1 mutations (deletions) carried by the Mut1/Spp1-/- line (other EMMA strain EM:15972) and the Mut15/DKO line (this EMMA strain EM:15971) are distinct, since one was generated on a wild-type chromosome, while the other one is located on a chromosome carrying the Ibsp knock-out mutation. The two genes are at short distance from each other on the same chromosome, hence the use of the TALEN tool in 2014. This is detailed in the genotyping procedure included with this strain submission. |
| References |
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| Homozygous fertile | yes |
| Homozygous viable | yes |
| Homozygous matings required | no |
| Immunocompromised | not known |
Information from EMMA
| Archiving centre | CNRS-TAAM – Typing and Archiving of Animal Models, Orléans, France |
| Animals used for archiving | homozygous CD1 males |
Disease and phenotype information
MGI phenotypes (gene matching)
- decreased bone mineral density / MGI
- large anterior fontanelle / MGI
- malocclusion / MGI
- abnormal trabecular bone morphology / MGI
- decreased compact bone thickness / MGI
- abnormal mandible morphology / MGI
- decreased body weight / MGI
- decreased body size / MGI
- abnormal molar morphology / MGI
- abnormal bone mineralization / MGI
- abnormal bone remodeling / MGI
- short femur / MGI
- delayed intramembranous bone ossification / MGI
- abnormal periodontal ligament morphology / MGI
- abnormal osteoclast morphology / MGI
- increased osteoclast cell number / MGI
- decreased osteoclast cell number / MGI
- abnormal osteoblast morphology / MGI
- decreased osteoblast cell number / MGI
- increased bone resorption / MGI
- abnormal incisor morphology / MGI
- craniofacial phenotype / MGI
- skeleton phenotype / MGI
- decreased trabecular bone thickness / MGI
- delayed cranial suture closure / MGI
- increased bone trabecula number / MGI
- increased trabecular bone volume / MGI
- abnormal osteoid morphology / MGI
- increased osteoid thickness / MGI
- abnormal tooth root development / MGI
- decreased bone trabecular spacing / MGI
- abnormal periodontium morphology / MGI
- wide coronal suture / MGI
- wide lambdoid suture / MGI
- delayed fontanelle closure / MGI
- abnormal cementum mineralization / MGI
- alveolar process atrophy / MGI
- abnormal molar root morphology / MGI
- abnormal junctional epithelium morphology / MGI
- abnormal tooth root resorption / MGI
- misaligned incisors / MGI
- abnormal acellular cementum morphology / MGI
- increased bone mineral density / MGI
- abnormal long bone metaphysis morphology / MGI
- abnormal microglial cell morphology / MGI
- decreased hematocrit / MGI
- decreased leukocyte cell number / MGI
- abnormal blood flow velocity / MGI
- abnormal blood vessel physiology / MGI
- increased bone marrow cell number / MGI
- altered response to myocardial infarction / MGI
- abnormal liver morphology / MGI
- abnormal substantia nigra morphology / MGI
- abnormal osteoclast physiology / MGI
- abnormal cardiovascular system physiology / MGI
- abnormal hematopoietic system physiology / MGI
- abnormal vasodilation / MGI
- abnormal blood vessel morphology / MGI
- abnormal immune system physiology / MGI
- altered susceptibility to infection / MGI
- abnormal inflammatory response / MGI
- decreased susceptibility to viral infection / MGI
- decreased susceptibility to bacterial infection / MGI
- increased susceptibility to bacterial infection / MGI
- abnormal blood cell morphology/development / MGI
- abnormal leukocyte physiology / MGI
- abnormal macrophage morphology / MGI
- abnormal macrophage physiology / MGI
- granulomatous inflammation / MGI
- increased heart rate / MGI
- decreased circulating triglyceride level / MGI
- dilated renal tubules / MGI
- decreased circulating insulin level / MGI
- decreased heart weight / MGI
- decreased systemic arterial blood pressure / MGI
- decreased hemoglobin content / MGI
- increased insulin sensitivity / MGI
- abnormal bone mineralization / MGI
- delayed wound healing / MGI
- abnormal leukocyte migration / MGI
- nephrocalcinosis / MGI
- nervous system phenotype / MGI
- abnormal physiological neovascularization / MGI
- impaired macrophage chemotaxis / MGI
- decreased macrophage cell number / MGI
- decreased lean body mass / MGI
- abnormal striatum morphology / MGI
- renal tubular necrosis / MGI
- decreased incidence of tumors by chemical induction / MGI
- increased hematopoietic stem cell number / MGI
- decreased susceptibility to experimental autoimmune uveoretinitis / MGI
- lung cysts / MGI
- abnormal vascular wound healing / MGI
- increased osteoclast cell number / MGI
- decreased osteoclast cell number / MGI
- decreased bone resorption / MGI
- abnormal osteoblast physiology / MGI
- increased lymphocyte cell number / MGI
- abnormal wound healing / MGI
- abnormal response to infection / MGI
- decreased acute inflammation / MGI
- decreased cardiac muscle contractility / MGI
- increased susceptibility to injury / MGI
- improved glucose tolerance / MGI
- decreased susceptibility to atherosclerosis / MGI
- renal/urinary system phenotype / MGI
- homeostasis/metabolism phenotype / MGI
- reproductive system phenotype / MGI
- skeleton phenotype / MGI
- increased macrophage cell number / MGI
- hyporesponsive to tactile stimuli / MGI
- increased circulating creatinine level / MGI
- decreased circulating glucose level / MGI
- increased blood urea nitrogen level / MGI
- decreased susceptibility to type IV hypersensitivity reaction / MGI
- increased lung weight / MGI
- calcified aortic valve / MGI
- decreased systemic arterial systolic blood pressure / MGI
- decreased urine sodium level / MGI
- decreased dendritic cell number / MGI
- decreased tumor necrosis factor secretion / MGI
- decreased interferon-gamma secretion / MGI
- decreased circulating interleukin-6 level / MGI
- increased interleukin-10 secretion / MGI
- decreased interleukin-12 secretion / MGI
- increased interleukin-4 secretion / MGI
- abnormal chemokine level / MGI
- increased physiological sensitivity to xenobiotic / MGI
- decreased physiological sensitivity to xenobiotic / MGI
- decreased sensitivity to induced cell death / MGI
- increased neuron number / MGI
- increased trabecular bone thickness / MGI
- crystalluria / MGI
- increased sensitivity to induced morbidity/mortality / MGI
- decreased susceptibility to bacterial infection induced morbidity/mortality / MGI
- increased respiratory quotient / MGI
- abnormal macrophage chemotaxis / MGI
- mortality/aging / MGI
- decreased susceptibility to dopaminergic neuron neurotoxicity / MGI
- decreased urine chloride ion level / MGI
- decreased fibroblast chemotaxis / MGI
Literature references
- OPN, BSP, and Bone Quality-Structural, Biochemical, and Biomechanical Assessment in OPN-/-, BSP-/-, and DKO Mice.;Malaval Luc, Follet Hélène, Farlay Delphine, Gineyts Evelyne, Rizzo Sebastien, Thomas Charlene, Maalouf Mathieu, Normand Myriam, Burt-Pichat Brigitte, Bouleftour Wafa, Vanden-Boscche Arnaud, Laroche Norbert, Vico Laurence, ;2024;Calcified tissue international;115;63-77; 38733411
- Deletion of osteopontin or bone sialoprotein induces opposite bone responses to mechanical stimulation in mice.;Maalouf M, Çinar H, Bouleftour W, Thomas M, Vanden-Bossche A, Laroche N, Linossier M T, Peyroche S, Lafage-Proust M H, Vico L, Guignandon A, Malaval L, ;2022;Bone reports;17;101621; 36159882
- Deletion of OPN in BSP knockout mice does not correct bone hypomineralization but results in high bone turnover.;Bouleftour W, Juignet L, Verdière L, Machuca-Gayet I, Thomas M, Laroche N, Vanden-Bossche A, Farlay D, Thomas C, Gineyts E, Concordet J P, Renaud J B, Aubert D, Teixeira M, Peyruchaud O, Vico L, Lafage-Proust M H, Follet H, Malaval L, ;2019;Bone;120;411-422; 30529011