Tetrahydropteridine deficiency impairs mitochondrial function in Dictyostelium discoideum Ax2.
A putative cellular function of tetrahydropteridines (l-erythro-tetrahydrobiopterin and d-threo-tetrahydrobiopterin) was investigated in Dictyostelium discoideum Ax2 using a mutant disrupted in the gene encoding sepiapterin reductase (SR). The SR mutant, which produces about 3% of tetrahydropteridines if compared to wild-type, was elucidated to have several functional defects related to mitochondria and oxidative stress: retarded growth, poor spore viability, impaired mitochondrial function, and increased susceptibility to oxidative stress induced by hydroxylamine or cumene-hydroperoxide. However, the physiological defects were almost completely rescued by extrachromosomal expression of Dictyostelium SR. The results strongly suggested that tetrahydropteridines in Dictyostelium are associated with mitochondrial function, probably via direct protection against oxidative stress.
Kim
Hye-Lim
HL
Mitochondrial Research Group, School of Biotechnology and Biomedical Science, Inje University, Kimhae 621-749, Republic of Korea.
Choi
Yong Kee
YK
Kim
Do Hyung
DH
Park
Sun Ok
SO
Han
Jin
J
Park
Young Shik
YS
D000818:Animals; D004023:Dictyostelium / Q000187:drug effects* / Q000254:growth & development / Q000378:metabolism*; D008928:Mitochondria / Q000378:metabolism*; D018384:Oxidative Stress; D011621:Pteridines / Q000494:pharmacology*; D033761:Spores, Protozoan / Q000187:drug effects / Q000254:growth & development
D011621:Pteridines; C045357:5,6,7,8-tetrahydropteridine