Model organisms
edit| Characteristic | Phenotype |
|---|---|
| Homozygote viability | Abnormal |
| Recessive lethal study | Normal |
| Fertility | Normal |
| Body weight | Abnormal[1] |
| Anxiety | Normal |
| Neurological assessment | Normal |
| Grip strength | Normal |
| Hot plate | Normal |
| Dysmorphology | Normal |
| Indirect calorimetry | Abnormal[2] |
| Glucose tolerance test | Abnormal[3] |
| Auditory brainstem response | Normal |
| DEXA | Abnormal[4] |
| Radiography | Abnormal[5] |
| Body temperature | Normal |
| Eye morphology | Normal |
| Clinical chemistry | Abnormal[6] |
| Haematology | Normal |
| Peripheral blood lymphocytes | Abnormal |
| Micronucleus test | Normal |
| Heart weight | Normal |
| Skin Histopathology | Normal |
| Brain histopathology | Normal |
| Eye Histopathology | Normal |
| Salmonella infection | Normal[7] |
| Citrobacter infection | Normal[8][9] |
| All tests and analysis from[10] |
Model organisms have been used in the study of AKAP9 function. A conditional knockout mouse line, called Akap9tm1a(KOMP)Wtsi[11][12] was generated as part of the International Knockout Mouse Consortium program — a high-throughput mutagenesis project to generate and distribute animal models of disease to interested scientists.[13][14][15]
Male and female animals underwent a standardized phenotypic screen to determine the effects of deletion.[10][16] Twenty six tests were carried out on mutant mice and eight significant abnormalities were observed.[10] Fewer than expected homozygous mutant mice survived until weaning. The remaining tests were carried out on both homozygous and heterozygous mutant adult mice. Animals of both sex displayed decreased body fat and body weight, hematopoietic abnormalities and an atypical plasma chemistry panel. Female homozygotes also displayed abnormal tooth morphology while males heterozygous animals displayed an abnormal pelvic girdle bone morphology.[10]
References
edit- ^ "Body weight data for Akap9". Wellcome Trust Sanger Institute.
- ^ "Indirect calorimetry data for Akap9". Wellcome Trust Sanger Institute.
- ^ "Glucose tolerance test data for Akap9". Wellcome Trust Sanger Institute.
- ^ "DEXA data for Akap9". Wellcome Trust Sanger Institute.
- ^ "Radiography data for Akap9". Wellcome Trust Sanger Institute.
- ^ "Clinical chemistry data for Akap9". Wellcome Trust Sanger Institute.
- ^ "Salmonella infection data for Akap9". Wellcome Trust Sanger Institute.
- ^ "Citrobacter infection data for Akap9". Wellcome Trust Sanger Institute.
- ^ Mouse Resources Portal, Wellcome Trust Sanger Institute.
- ^ a b c d Gerdin AK (2010). "The Sanger Mouse Genetics Programme: high throughput characterisation of knockout mice". Acta Opthalmologica 88: 925-7.doi:10.1111/j.1755-3768.2010.4142.x: Wiley.
{{cite web}}: CS1 maint: location (link) - ^ "International Knockout Mouse Consortium".
- ^ "Mouse Genome Informatics".
- ^ Skarnes, W. C.; Rosen, B.; West, A. P.; Koutsourakis, M.; Bushell, W.; Iyer, V.; Mujica, A. O.; Thomas, M.; Harrow, J.; Cox, T.; Jackson, D.; Severin, J.; Biggs, P.; Fu, J.; Nefedov, M.; De Jong, P. J.; Stewart, A. F.; Bradley, A. (2011). "A conditional knockout resource for the genome-wide study of mouse gene function". Nature. 474 (7351): 337–342. doi:10.1038/nature10163. PMC 3572410. PMID 21677750.
- ^ Dolgin E (June 2011). "Mouse library set to be knockout". Nature 474: 262-263. doi:10.1038/474262a.
{{cite web}}: CS1 maint: location (link) CS1 maint: year (link) - ^ Collins FS, Rossant J, Wurst W (January 2007). A mouse for all reasons. Cell 128(1): 9-13. doi:10.1016/j.cell.2006.12.018 PMID 17218247.
{{cite book}}: CS1 maint: location (link) CS1 maint: location missing publisher (link) CS1 maint: multiple names: authors list (link) CS1 maint: year (link) - ^ van der Weyden L, White JK, Adams DJ, Logan DW (2011). "The mouse genetics toolkit: revealing function and mechanism". Genome Biol. 12 (6): 224. doi:10.1186/gb-2011-12-6-224. PMID 21722353.
{{cite journal}}: CS1 maint: multiple names: authors list (link) CS1 maint: unflagged free DOI (link)