Expressing the multifunctional nucleoside kinase of Drosophila melanogaster in a mouse model : a strategy to reverse the depletion of mtDNA caused by nucleoside kinase deficiency
Independent thesis Advanced level (degree of Master (Two Years)), 60 credits / 90 HE creditsStudent thesis
This study was initiated to investigate a possible strategy to alter an enzyme deficiency in a mouse model. The enzyme investigated is a multifunctional nucleoside kinase from Drosophila melanogaster (Dm-dNK). This enzyme has special features in that it has higher enzymatic activity than any other known nucleoside kinases and still has similar substrate specificity as the human nucleoside kinases. The deficiency where the Dm-dNK transgenic mice model will be used is a TK2 deficient model with severe phenotype caused by mitochondrial DNA depletion. The Dm-dNK transgenic mice model will be used as a way to rescue the TK2 deficient mice. The results from the present study show that Dm-dNK expression in mice results in a substantial increase of thymidine phosphorylation in several investigated tissues. The mice were otherwise normal as judged by life span, weight and behavior. The mitochondrial DNA was also detected at normal levels. In conclusion, the Dm-dNK mouse model is promising as a way to rescue the severe phenotype of the TK2 deficient mice.
Place, publisher, year, edition, pages
2011. , 15 p.
Dm-dNK, mitochondria, thymidine kinase, phosphorylation
Engineering and Technology
IdentifiersURN: urn:nbn:se:liu:diva-69147ISRN: LiTH-IFM-A-EX--11/2432—SEOAI: oai:DiVA.org:liu-69147DiVA: diva2:424166
Subject / course
2011-05-27, BL32, Linkoping, 10:18 (English)
Karlsson, Anna, Professor
Altimiras, Jordi, Associate Professor