SLC25A29

Solute carrier family 25, member 29 is a protein that in humans is encoded by the SLC25A29 gene.[1] The gene is also known as CACL and C14orf69.[1] SLC25A29 belongs to a protein family of solute carriers called the mitochondrial carriers.[1]

Model organisms

Slc25a29 knockout mouse phenotype

Characteristic	Phenotype
Homozygote viability	Normal
Fertility	Normal
Body weight	Normal
Anxiety	Normal
Neurological assessment	Normal
Grip strength	Normal
Hot plate	Normal
Dysmorphology	Normal
Indirect calorimetry	Normal
Glucose tolerance test	Normal
Auditory brainstem response	Normal
DEXA	Normal
Radiography	Normal
Body temperature	Normal
Eye morphology	Normal
Clinical chemistry	Normal
Haematology	Normal
Peripheral blood lymphocytes	Normal
Micronucleus test	Normal
Heart weight	Normal
Skin Histopathology	Normal
Brain histopathology	Normal
Salmonella infection	Normal[2]
Citrobacter infection	Normal[3]
All tests and analysis from[4][5]

Model organisms have been used in the study of SLC25A29 function. A conditional knockout mouse line, called Slc25a29^{tm1a(KOMP)Wtsi}[6][7] 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 — at the Wellcome Trust Sanger Institute.[8][9][10]

Male and female animals underwent a standardized phenotypic screen to determine the effects of deletion.[4][11] Twenty four tests were carried out on mutant mice, but no significant abnormalities were observed.[4]

References

1. "Solute carrier family 25, member 29". Retrieved 2011-12-05.
2. "Salmonella infection data for Slc25a29". Wellcome Trust Sanger Institute.
3. "Citrobacter infection data for Slc25a29". Wellcome Trust Sanger Institute.
4. Gerdin AK (2010). "The Sanger Mouse Genetics Programme: High throughput characterisation of knockout mice". Acta Ophthalmologica. 88 (S248). doi:10.1111/j.1755-3768.2010.4142.x.
5. Mouse Resources Portal, Wellcome Trust Sanger Institute.
6. "International Knockout Mouse Consortium".
7. "Mouse Genome Informatics".
8. 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.
9. Dolgin E (June 2011). "Mouse library set to be knockout". Nature. 474 (7351): 262–3. doi:10.1038/474262a. PMID 21677718.
10. 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.
11. 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. PMC 3218837. PMID 21722353.

Further reading

• Camacho, J. E. A.; Rioseco-Camacho, N. (2009). "The Human and Mouse SLC25A29 Mitochondrial Transporters Rescue the Deficient Ornithine Metabolism in Fibroblasts of Patients with the Hyperornithinemia-Hyperammonemia-Homocitrullinuria (HHH) Syndrome". Pediatric Research. 66 (1): 35–41. doi:10.1203/PDR.0b013e3181a283c1. PMID 19287344.
• Sekoguchi, E.; Sato, N.; Yasui, A.; Fukada, S.; Nimura, Y.; Aburatani, H.; Ikeda, K.; Matsuura, A. (2003). "A Novel Mitochondrial Carnitine-acylcarnitine Translocase Induced by Partial Hepatectomy and Fasting". Journal of Biological Chemistry. 278 (40): 38796–38802. doi:10.1074/jbc.M306372200. PMID 12882971.