Chlamydomonas reinhardtii as a plant model system to study mitochondrial complex I dysfunction.

ABSTRACT: Mitochondrial complex I, a proton-pumping NADH: ubiquinone oxidoreductase, is required for oxidative phosphorylation. However, the contribution of several human mutations to complex I deficiency is poorly understood. The unicellular alga Chlamydomonas reinhardtii was utilized to study complex I as, unlike in mammals, mutants with complete loss of the holoenzyme are viable. From a forward genetic screen for complex I-deficient insertional mutants, six mutants exhibiting complex I deficiency with assembly defects were isolated. Chlamydomonas mutants isolated from our screens, lacking the subunits NDUFV2 and NDUFB10, were used to reconstruct and analyze the effect of two human mutations in these subunit-encoding genes. The K209R substitution in NDUFV2, reported in Parkinson's disease patients

SUBMITTER: Subrahmanian N 

PROVIDER: S-EPMC6996877 | biostudies-literature | 2020 Feb

REPOSITORIES: biostudies-literature