GATC (gene)
Glutamyl-tRNA(Gln) amidotransferase, subunit C homolog (bacterial) is a protein that in humans is encoded by the GATC gene.[1] The gene is also known as 15E1.2 and encodes part of a Glu-tRNA(Gln) amidotransferase enzyme.[1]
Model organisms
Characteristic | Phenotype |
---|---|
Homozygote viability | Abnormal |
Recessive lethal study | Abnormal |
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 |
Plasma immunoglobulins | Normal |
Haematology | Normal |
Peripheral blood lymphocytes | Normal |
Micronucleus test | Normal |
Heart weight | Normal |
Tail epidermis wholemount | Normal |
Skin Histopathology | Normal |
Brain histopathology | Normal |
Eye 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 GATC function. A conditional knockout mouse line, called Gatctm1a(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 eight tests were carried out on mutant mice and two significant abnormalities were observed.[4] No homozygous mutant embryos were recorded during gestation and, in a separate study, no homozygous animals were observed at weaning. This may imply that double deletion of the GATC gene is lethal to zygotes. The remaining tests were carried out on adult heterozygous mutant animals but no further abnormalities were seen.[4]
References
- "Glutamyl-tRNA(Gln) amidotransferase, subunit C homolog (bacterial)". Retrieved 2011-12-07.
- "Salmonella infection data for Gatc". Wellcome Trust Sanger Institute.
- "Citrobacter infection data for Gatc". Wellcome Trust Sanger Institute.
- 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. S2CID 85911512.
- Mouse Resources Portal, Wellcome Trust Sanger Institute.
- "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 (7351): 262–3. doi:10.1038/474262a. PMID 21677718.
- 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. S2CID 18872015.
- 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
- Nagao, A.; Suzuki, T.; Katoh, T.; Sakaguchi, Y.; Suzuki, T. (2009). "Biogenesis of glutaminyl-mt tRNAGln in human mitochondria". Proceedings of the National Academy of Sciences. 106 (38): 16209–16214. Bibcode:2009PNAS..10616209N. doi:10.1073/pnas.0907602106. PMC 2752530. PMID 19805282.