Mouse Strain information
APB ID 2783
Added 16/02/2008
Last Edited 24/04/2015
Strain name: B6(Cg)-Clec2dtm1.1Mgil/Apb
Nickname: C57BL/6.OCIL-KO
Strain designation name: B6(Cg)-Clec2dtm1.1Mgil/Apb
Genetics
Strain Types Mutant strain
Genetic Details Targeted knockout
ES Cell-Line Used C57BL/6
Mode of Inheritance Recessive
1.  Affected Gene Name: C-type lectin domain family 2, member d  
Chromosome 6
Affected Gene Symbol Clec2d
Protein expression of altered gene: Unknown
Genetic alteration of gene: A loxP site was inserted upstream of exon 3 and a downstream floxed neo cassettes was inserted downstream of exon 3. Chimeric progeny were bred with a cre deleter strain to remove exon 3, leaving behind a single loxP site. Gene inactivation was confirmed by Southern blotting of cDNA derived from tail mRNA. Expression levels of Clec2g and Clec2i genes were unaffected in these mice.
Location on chromosome (bp): 129130633-129136552 bp, + strand (From VEGA annotation of NCBI Build 37)
MGI Gene Accession ID

Please also use this link to determine if other mutants have been registered with MGI (Mouse Genome Informatics)

MGI:2135589
Synonyms Clr-b, Clrb, Ocil
Allele Name targeted mutation 1.1, Matthew T Gillespie
Allele Symbol Clec2dtm1.1Mgil
MGI Allele Accession ID MGI:3826396
Mutant Construction Technique None
Phenotype
Phenotype Homozygous State The mice show no overt phenotype. The bone phenotype (as analysed by bone histomorphometry) is mild "osteopenia" or a low bone mass due to a high bone turnover (caused by increased numbers of osteoclasts).
Phenotype Heterozygous State Not examined
Original Genetic Background C57BL/6 x 129Sv
Genetic Background Currently Maintained C57BL/6
Coat Colour Black
Eye Colour Black
Strain Images
Trabecular bone structure in OCIL<-/-> and WT contol mice. Representative sections of proximal tibiae of WT control and OCIL<-/-> mice at 16 weeks of age strained with modified Von Kossa stain (mineralised bone is stained black).
Trabecular bone structure in OCIL-/- and WT contol mice. Representative sections of proximal tibiae of WT control and OCIL-/- mice at 16 weeks of age strained with modified Von Kossa stain (mineralised bone is stained black).
Targeted disruption of ocil. (A) Schematic representation of the targeting construct showing the wild type allele
at the top and the targeted allele at the bottom. Exons 1, 2, 3, 4 and 5 of ocil are depicted as rectangles. The targeting
construct containing a PGK gene cassette and a neomycin (Neo) resistance gene cassette is depicted. The neo cassette and
exon 3 are both flanked by LoxP sites. Construction of the ocil-/- targeting vector involved the excision of exon 3 of the
ocil gene. Due to deletion of this exon, any read-through transcripts of ocil that may arise due to splicing of exons 2 to 4,
or exons 2 to 5 result in the introduction of a frame-shift, and therefore a non-functional transcript of ocil and a resultant
inactive protein.
Targeted disruption of ocil. (A) Schematic representation of the targeting construct showing the wild type allele at the top and the targeted allele at the bottom. Exons 1, 2, 3, 4 and 5 of ocil are depicted as rectangles. The targeting construct containing a PGK gene cassette and a neomycin (Neo) resistance gene cassette is depicted. The neo cassette and exon 3 are both flanked by LoxP sites. Construction of the ocil-/- targeting vector involved the excision of exon 3 of the ocil gene. Due to deletion of this exon, any read-through transcripts of ocil that may arise due to splicing of exons 2 to 4, or exons 2 to 5 result in the introduction of a frame-shift, and therefore a non-functional transcript of ocil and a resultant inactive protein.
Strain identification
How is this strain characterised? Genotyping
PCR protocols B6-OCIL-KO (touch-down RT-PCR - OCILrp1/rp2 primers)
B6-OCIL-KO (GAPDH internal control)
Fertility and Strain maintenance
Fertility and Strain maintenance
Relevant bibliographic / database references
Strain Specific References
Other Related References
General information
Other Patent Technologies? Discovery of the Deil gene was patented in 1999 [Patent Application: Australian Patent Application No. 57975/00, Accepted No. 780470, Provisional Patent Application No. PQ1675. International Publication Number WO 01105964 AI. Date of filing: Australia Provisional 19.07.99. Worldwide filing 19.07.00, International Publication Date 25.01.2001, National Phase Entry 25.01.2002, accepted Australian Patent Office 08/02/05.
Associated IP rights? Yes
Does it Model a Human Condition? Unknown
Research value of this Strain B6-0CIL-KO is the only strain ever generated by a laboratory to demonstrate the loss of a C-type lectin (shown to have actions in bone biology)
Applicable Research Areas Cell biology
Cancer
Immunology and inflammation
Keywords
  • c-type lectin
  • osteoclast
  • bone remodelling
  • natural killer cell
Additional Information The Osteoclast Inhibitory Lectin (OCIL) protein is a type II transmembrane C-type lectin that belongs to the Natural Killer cell receptor group and is known to inhibit the formation of bone-resorbing cells "osteoclasts" (JBC ref 2001) as well as have negative effects on mesenchymal-derived cells such as the bone-forming cells "osteoblasts" and adipocytes (Bone ref 2007). Construction of the "OCIL knock-out" targeting vector involved excision of exon 3, any readthrough transcripts of OCIL that may arise due to splicing of exons 2 to 4, or exons 2 to 5 results in the introduction of a frame-shift, and therefore a non-functional transcript of OCIL and a resultant inactive protein. Exon 2 encodes the transmembrane domain of the OCIL gene and exon 3 encodes the C-terminal end of the extracellular domain. The anticipated effect of "knocking-out" the OCIL gene in mice was an osteoporotic bone phenotype however in our case these mice only display a mild osteopenia. The most likely reason for this is "redundancy" from the other OCIL related proteins (OCILrpl/2) which were not ablated during the generation of the OCIL-KO mice. Long bones of 10 and l6-week old ocil-/- mice have increased osteoclast surface and numbers which is indicative of high levels of bone resorption as anticipated. Other bone parameters as measured by Von Kossa staining and histomorphometry demonstrate a lower tibial trabecular bone volume, lower trabecular thickness and decreased trabecular number in 10 and 16-week old male ocil-/- mice compared to wt controls. Serum calcium levels are significantly elevated in both male and female 16-week old ocil-/- mice while serum PTH levels are significantly lower in both 10- week and 16-week:old ocil-/- mice. So these data suggest that the absence of OCIL in vivo results in low bone mass mainly due to a high bone turnover (increased numbers of osteoclasts) and these mice are the first to demonstrate a significant role for a NK cell C-type lectin in bone metabolism in vivo.
Is the strain available in any form to other researchers Yes
APB stock stored as: Cryopreserved sperm (from 10 mice)

APB stock genotyped verified by: The depositor
Are live mice available? Unknown
MTA needs to be signed? Yes


   

 


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