No abstract

Mitochondrial dysfunction elicits stress responses that safeguard cellular homeostasis against metabolic insults. Mitochondrial integrated stress response (ISR mt) is a major response to mitochondrial (mt)DNA expression stress (mtDNA maintenance, translation defects), but knowledge of dynamics or interdependence of components is lacking. We report that in mitochondrial myopathy ISR mt progresses in temporal stages, and development from early to chronic is regulated by autocrine and endocrine effects of FGF21, a metabolic hormone with pleiotropic effects. Initial disease signs induce transcriptional ISR mt (ATF5, mitochondrial one-carbon cycle, FGF21, GDF15). The local progression to 2 nd metabolic ISR mt-stage (ATF3, ATF4, glucose uptake, serine biosynthesis, transsulfuration) is FGF21-dependent. Mitochondrial unfolded protein response marks the 3 rd ISR mtstage of failing tissue. Systemically, FGF21 drives weight-loss, glucose-preference and modifies metabolism and respiratory chain deficiency in a specific hippocampal brain region. Our evidence indicates that FGF21 is a local and systemic messenger of mtDNA stress in mice and humans with mitochondrial disease.

No abstract

Strained GaSb quantum dots having a staggered band lineup (type II) are formed in a GaAs matrix using molecular beam epitaxy. The dots are growing in a self-organized way on a GaAs(100) surface upon deposition of 1.2 nm GaSb followed by a GaAs cap layer. Plan-view transmission electron microscopy studies reveal well developed rectangular-shaped GaSb islands with a lateral extension of ∼20 nm. Intense photoluminescence (PL) is observed at an energy lower than the GaSb wetting layer luminescence. This line is attributed to radiative recombination of 0D holes located in the GaSb dots and electrons located in the surrounding regions. The GaSb quantum dot PL dominates the spectrum up to high excitation densities and up to room temperature.