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

Gatc knockout mouse phenotype

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 Gatc^{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 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

1. "Glutamyl-tRNA(Gln) amidotransferase, subunit C homolog (bacterial)" . Retrieved 2011-12-07.
2. "Salmonella infection data for Gatc". Wellcome Trust Sanger Institute.
3. "Citrobacter infection data for Gatc". 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. S2CID   85911512.
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. S2CID   18872015.
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

• 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.