Jan Hegermann

TL;DR: It is demonstrated with in vitro vesicle fusion experiments that αS has an inhibitory function on membrane fusion and mitochondrial fragmentation induced by expression of αS is rescued by coexpression of PINK1, parkin or DJ‐1 but not the PD‐associated mutations Pink1 G309D and parkin Δ1–79 or byDJ‐1 C106A.

TL;DR: It is demonstrated that a mutation in the Caenorhabditits elegans homologue of the PTEN-induced kinase pink-1 gene resulted in reduced mitochondrial cristae length and increased paraquat sensitivity of the nematode, and the first evidence of an antagonistic role of PINK-1 and LRK-1 is provided.

TL;DR: TFG-1 is identified, a new conserved regulator of protein secretion that interacts directly with SEC-16 and controls the export of cargoes from the endoplasmic reticulum in Caenorhabditis elegans, providing a mechanism by which translocations involving TFG can result in cellular transformation and oncogenesis.

TL;DR: The data show a functional role for endoplasmic reticulum-localized PIN8 and suggest a mechanism whereby PIN8 controls auxin thresholds and access of auxin to the nucleus, thereby regulating auxin-dependent transcriptional activity.

TL;DR: Double-homozygous mutants of tardbp and tardbpl show muscle degeneration, strongly reduced blood circulation, mispatterning of vessels, impaired spinal motor neuron axon outgrowth, and early death in double mutants the muscle-specific actin binding protein Filamin Ca is up-regulated.