The curious case of the Dana platypus and what it can teach us about how lead shotgun pellets behave in fluid preserved museum specimens and may limit their scientific value.

Fluid preserved animal specimens in the collections of natural history museums constitute an invaluable archive of past and present animal diversity. Well-preserved specimens have a shelf-life spanning centuries and are widely used for e.g.

ESYT1 tethers the ER to mitochondria and is required for mitochondrial lipid and calcium homeostasis.

Mitochondria interact with the ER at structurally and functionally specialized membrane contact sites known as mitochondria-ER contact sites (MERCs). Combining proximity labelling (BioID), co-immunoprecipitation, confocal microscopy and subcellular fractionation, we found that the ER resident SMP-domain protein ESYT1 was enriched at MERCs, where it forms a complex with the outer mitochondrial membrane protein SYNJ2BP. BioID analyses using ER-targeted, outer mitochondrial membrane-targeted, and MERC-targeted baits, confirmed the presence of this complex at MERCs and the specificity of the interaction.

MIROs and DRP1 drive mitochondrial-derived vesicle biogenesis and promote quality control.

Mitochondrial-derived vesicles (MDVs) are implicated in diverse physiological processes-for example, mitochondrial quality control-and are linked to various neurodegenerative diseases. However, their specific cargo composition and complex molecular biogenesis are still unknown. Here we report the proteome and lipidome of steady-state TOMM20 MDVs.

The enigma of an interconnected mitochondrial reticulum: new insights into mitochondrial fusion.

It has been over 20 years since the identification of the first GTPases that regulate mitochondrial fusion in drosophila, yeast, and mammalian cells. While the molecular identification of these players solidified the new field of mitochondrial dynamics, cell imaging had established the dynamic properties of mitochondria over a century before. The genetic dissection of mitochondrial fusion, fission, and positioning within cells cemented our understanding of the essential nature of this plasticity in health and disease.

Sensory neuropathy-causing mutations in ATL3 affect ER-mitochondria contact sites and impair axonal mitochondrial distribution.

Axonopathies are neurodegenerative disorders caused by axonal degeneration, affecting predominantly the longest neurons. Several of these axonopathies are caused by genetic defects in proteins involved in the shaping and dynamics of the endoplasmic reticulum (ER); however, it is unclear how these defects impinge on neuronal survival. Given its central and widespread position within a cell, the ER is a pivotal player in inter-organelle communication.