216 research outputs found
Disk Detective: Discovery of New Circumstellar Disk Candidates through Citizen Science
The Disk Detective citizen science project aims to find new stars with 22
micron excess emission from circumstellar dust using data from NASA's WISE
mission. Initial cuts on the AllWISE catalog provide an input catalog of
277,686 sources. Volunteers then view images of each source online in 10
different bands to identify false-positives (galaxies, background stars,
interstellar matter, image artifacts, etc.). Sources that survive this online
vetting are followed up with spectroscopy on the FLWO Tillinghast telescope.
This approach should allow us to unleash the full potential of WISE for finding
new debris disks and protoplanetary disks. We announce a first list of 37 new
disk candidates discovered by the project, and we describe our vetting and
follow-up process. One of these systems appears to contain the first debris
disk discovered around a star with a white dwarf companion: HD 74389. We also
report four newly discovered classical Be stars (HD 6612, HD 7406, HD 164137,
and HD 218546) and a new detection of 22 micron excess around a previously
known debris disk host star, HD 22128.Comment: 50 pages, accepted for publication in the Astrophysical Journa
Protein Phase Separation: A New Phase in Cell Biology
Cellular compartments and organelles organize biological matter. Most well-known organelles are separated by a membrane boundary from their surrounding milieu. There are also many so-called membraneless organelles and recent studies suggest that these organelles, which are supramolecular assemblies of proteins and RNA molecules, form via protein phase separation. Recent discoveries have shed light on the molecular properties, formation, regulation, and function of membraneless organelles. A combination of techniques from cell biology, biophysics, physical chemistry, structural biology, and bioinformatics are starting to help establish the molecular principles of an emerging field, thus paving the way for exciting discoveries, including novel therapeutic approaches for the treatment of age-related disorders. © 201
AMPK activation promotes lipid droplet dispersion on detyrosinated microtubules to increase mitochondrial fatty acid oxidation
Lipid droplets (LDs) are intracellular organelles that provide fatty acids (FAs) to cellular processes including synthesis of membranes and production of metabolic energy. While known to move bidirectionally along microtubules (MTs), the role of LD motion and whether it facilitates interaction with other organelles are unclear. Here we show that during nutrient starvation, LDs and mitochondria relocate on detyrosinated MT from the cell centre to adopt a dispersed distribution. In the cell periphery, LD-mitochondria interactions increase and LDs efficiently supply FAs for mitochondrial beta-oxidation. This cellular adaptation requires the activation of the energy sensor AMPK, which in response to starvation simultaneously increases LD motion, reorganizes the network of detyrosinated MTs and activates mitochondria. In conclusion, we describe the existence of a specialized cellular network connecting the cellular energetic status and MT dynamics to coordinate the functioning of LDs and mitochondria during nutrient scarcity
C9orf72-derived arginine-containing dipeptide repeats associate with axonal transport machinery and impede microtubule-based motility
A hexanucleotide repeat expansion in the C9orf72 gene is the most common genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). How this mutation leads to these neurodegenerative diseases remains unclear. Here, we show using patient stem cell-derived motor neurons that the repeat expansion impairs microtubule-based transport, a process critical for neuronal survival. Cargo transport defects are recapitulated by treating neurons from healthy individuals with proline-arginine and glycine-arginine dipeptide repeats (DPRs) produced from the repeat expansion. Both arginine-rich DPRs similarly inhibit axonal trafficking in adult Drosophila neurons in vivo. Physical interaction studies demonstrate that arginine-rich DPRs associate with motor complexes and the unstructured tubulin tails of microtubules. Single-molecule imaging reveals that microtubule-bound arginine-rich DPRs directly impede translocation of purified dynein and kinesin-1 motor complexes. Collectively, our study implicates inhibitory interactions of arginine-rich DPRs with axonal transport machinery in C9orf72-associated ALS/FTD and thereby points to potential therapeutic strategies.</p
C9orf72 -derived arginine-containing dipeptide repeats associate with axonal transport machinery and impede microtubule-based motility
C9orf72-derived arginine-containing dipeptide repeats associate with axonal transport machinery and impede microtubule-based motility
A hexanucleotide repeat expansion in the C9orf72 gene is the most common genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). How this mutation leads to these neurodegenerative diseases remains unclear. Here, we show using patient stem cell-derived motor neurons that the repeat expansion impairs microtubule-based transport, a process critical for neuronal survival. Cargo transport defects are recapitulated by treating neurons from healthy individuals with proline-arginine and glycine-arginine dipeptide repeats (DPRs) produced from the repeat expansion. Both arginine-rich DPRs similarly inhibit axonal trafficking in adult Drosophila neurons in vivo. Physical interaction studies demonstrate that arginine-rich DPRs associate with motor complexes and the unstructured tubulin tails of microtubules. Single-molecule imaging reveals that microtubule-bound arginine-rich DPRs directly impede translocation of purified dynein and kinesin-1 motor complexes. Collectively, our study implicates inhibitory interactions of arginine-rich DPRs with axonal transport machinery in C9orf72-associated ALS/FTD and thereby points to potential therapeutic strategies.</p
Expanding Antarctic biogeography: microbial ecology of Antarctic island soils
The majority of islands surrounding the Antarctic continent are poorly characterized in terms of microbial macroecology due to their remote locations, geographical isolation and access difficulties. The 2016/2017 Antarctic Circumnavigation Expedition (ACE) provided unprecedented access to a number of these islands. In the present study we use metagenomic methods to investigate the microbial ecology of soil samples recovered from 11 circum-Antarctic islands as part of ACE, and to investigate the functional potential of their soil microbial communities. Comparisons of the prokaryote and lower eukaryote phylogenetic compositions of the soil communities indicated that the various islands harbored spatially distinct microbiomes with limited overlap. In particular, we identified a high prevalence of lichen-associated fungal taxa in the soils, suggesting that terrestrial lichens may be one of the key drivers of soil microbial ecology on these islands. Differential abundance and redundancy analyses suggested that these soil microbial communities are also strongly shaped by multiple abiotic factors, including soil pH and average annual temperatures. Most importantly, we demonstrate that the islands sampled in this study can be clustered into three distinct large-scale biogeographical regions in a conservation context, the sub-, Maritime and Continental Antarctic, which are distinct in both environmental conditions and microbial ecology, but are consistent with the widely-used regionalization applied to multicellular Antarctic terrestrial organisms. Functional profiling of the island soil metagenomes from these three broad biogeographical regions also suggested a degree of functional differentiation, reflecting their distinct microbial ecologies. Taken together, these results represent the most extensive characterization of the microbial ecology of Antarctic island soils to date
Acyl-CoA synthetase 3 promotes lipid droplet biogenesis in ER microdomains
Control of lipid droplet (LD) nucleation and copy number are critical, yet poorly understood, processes. We use model peptides that shift from the endoplasmic reticulum (ER) to LDs in response to fatty acids to characterize the initial steps of LD formation occurring in lipid-starved cells. Initially, arriving lipids are rapidly packed in LDs that are resistant to starvation (pre-LDs). Pre-LDs are restricted ER microdomains with a stable core of neutral lipids. Subsequently, a first round of “emerging” LDs is nucleated, providing additional lipid storage capacity. Finally, in proportion to lipid concentration, new rounds of LDs progressively assemble. Confocal microscopy and electron tomography suggest that emerging LDs are nucleated in a limited number of ER microdomains after a synchronized stepwise process of protein gathering, lipid packaging, and recognition by Plin3 and Plin2. A comparative analysis demonstrates that the acyl-CoA synthetase 3 is recruited early to the assembly sites, where it is required for efficient LD nucleation and lipid storag
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