Seedling traits, plasticity and local differentiation as strategies of invasive species of Impatiens in central Europe.

Background And Aims: Invasiveness of some alien plants is associated with their traits, plastic responses to environmental conditions and interpopulation differentiation. To obtain insights into the role of these processes in contributing to variation in performance, we compared congeneric species of Impatiens (Balsaminaceae) with different origin and invasion status that occur in central Europe.

Methods: Native I.

Expression and processing of the TMEM70 protein.

TMEM70 protein represents a novel ancillary factor of mammalian ATP synthase. We have investigated import and processing of this factor in human cells using GFP- and FLAG-tagged forms of TMEM70 and specific antibodies. TMEM70 is synthesized as a 29kDa precursor protein that is processed to a 21kDa mature form.

Mitochondrial ATP synthase deficiency due to a mutation in the ATP5E gene for the F1 epsilon subunit.

F1Fo-ATP synthase is a key enzyme of mitochondrial energy provision producing most of cellular ATP. So far, mitochondrial diseases caused by isolated disorders of the ATP synthase have been shown to result from mutations in mtDNA genes for the subunits ATP6 and ATP8 or in nuclear genes encoding the biogenesis factors TMEM70 and ATPAF2. Here, we describe a patient with a homozygous p.

Knockdown of F1 epsilon subunit decreases mitochondrial content of ATP synthase and leads to accumulation of subunit c.

The subunit epsilon of mitochondrial ATP synthase is the only F1 subunit without a homolog in bacteria and chloroplasts and represents the least characterized F1 subunit of the mammalian enzyme. Silencing of the ATP5E gene in HEK293 cells resulted in downregulation of the activity and content of the mitochondrial ATP synthase complex and of ADP-stimulated respiration to approximately 40% of the control. The decreased content of the epsilon subunit was paralleled by a decrease in the F1 subunits alpha and beta and in the Fo subunits a and d while the content of the subunit c was not affected.

TMEM70 mutations cause isolated ATP synthase deficiency and neonatal mitochondrial encephalocardiomyopathy.

We carried out whole-genome homozygosity mapping, gene expression analysis and DNA sequencing in individuals with isolated mitochondrial ATP synthase deficiency and identified disease-causing mutations in TMEM70. Complementation of the cell lines of these individuals with wild-type TMEM70 restored biogenesis and metabolic function of the enzyme complex. Our results show that TMEM70 is involved in mitochondrial ATP synthase biogenesis in higher eukaryotes.