Deficiency of Arabidopsis thaliana frataxin alters mitochondrial Fe-S proteins activity and induces oxidative stress

BUSI, MARIA VICTORIA; MALIANDI, MARIA VICTORIA; VALDEZ, HUGO ALBERTO; CLEMENTE, MARINA; ZABALETA, EDUARDO; ARAYA, ALEJANDRO; GOMEZ CASATI, DIEGO

PLANT JOURNAL

Blackwell Publishing Ltd

Año: 2006 vol. 48 p. 873 - 882

0960-7412

Frataxin, a protein crucial for the biogenesis of mitochondria in different organisms, was recently identified inArabidopsis thaliana. To investigate the role of frataxin in higher plants, we analyze two knock-out and oneknock-down T-DNA insertionmutants. The knock-outmutants present an embryo-lethal phenotype, indicatingan essential role for frataxin. The knock-down mutant has reduced frataxin mRNA and protein levels. Thismutant also presents retarded growth, reduced fresh weight of fruits and reduced number of seeds per fruit.Surprisingly, transcription of aconitase and the Fe?S subunit of succinate dehydrogenase (SDH2-1) areincreased in mutant plants; however, the activity of these proteins is reduced, indicating a role for frataxin inFe?S cluster assembly or insertion of Fe?S clusters into proteins. Mutant plants also have increased CO2assimilation rates, exhibit increased formation of reactive oxygen species (ROS) and have increased levels oftranscripts for proteins known to be involved in the ROS stress responses. These results indicate that frataxinis an essential protein in plants, required for full activity of mitochondrial Fe?S proteins and playing aprotective role against oxidative damage.