Generation and decay of Higgs mode in a strongly interacting Fermi gas.

We investigate the life cycle of the large amplitude Higgs mode in strongly interacting superfluid Fermi gas. Through numerical simulations with time-dependent density functional theory and the technique of the interaction quench, we verify the previous theoretical predictions on the mode's frequency. Next, we demonstrate that the mode is dynamically unstable against external perturbation and qualitatively examine the emerging state after the mode decays.

Dissipative Dynamics of Quantum Vortices in Fermionic Superfluid.

In a recent article, Kwon et al. [Nature (London) 600, 64 (2021)NATUAS0028-083610.1038/s41586-021-04047-4] revealed nonuniversal dissipative dynamics of quantum vortices in a fermionic superfluid.

Mitochondrial dysfunction reactivates α-fetoprotein expression that drives copper-dependent immunosuppression in mitochondrial disease models.

Signaling circuits crucial to systemic physiology are widespread, yet uncovering their molecular underpinnings remains a barrier to understanding the etiology of many metabolic disorders. Here, we identified a copper-linked signaling circuit activated by disruption of mitochondrial function in the murine liver or heart that resulted in atrophy of the spleen and thymus and caused a peripheral white blood cell deficiency. We demonstrated that the leukopenia was caused by α-fetoprotein, which required copper and the cell surface receptor CCR5 to promote white blood cell death.

Homoharringtonine demonstrates a cytotoxic effect against triple-negative breast cancer cell lines and acts synergistically with paclitaxel.

The lack of targeted therapies for triple-negative breast cancer (TNBC) contributes to their high mortality rates and high risk of relapse compared to other subtypes of breast cancer. Most TNBCs (75%) have downregulated the expression of CREB3L1 (cAMP-responsive element binding protein 3 like 1), a transcription factor and metastasis suppressor that represses genes that promote cancer progression and metastasis. In this report, we screened an FDA-approved drug library and identified four drugs that were highly cytotoxic towards HCC1806 CREB3L1-deficient TNBC cells.

Homeostatic control of nuclear-encoded mitochondrial gene expression by the histone variant H2A.Z is essential for neuronal survival.

Histone variants are crucial regulators of chromatin structure and gene transcription, yet their functions within the brain remain largely unexplored. Here, we show that the H2A histone variant H2A.Z is essential for neuronal survival.

Mouvement de passage: Creating connections through movement among persons with dementia.

One of the challenging consequences of dementia is the change in relationships that can co-occur with the progression of this condition. Despite this well-documented change, few arts-based interventions target the relational dimension of dementia. This study aims to explore the effects of one arts-based relational intervention: a movement program designed to foster connections within a group of persons with dementia.

Mitochondrial copper and phosphate transporter specificity was defined early in the evolution of eukaryotes.

The mitochondrial carrier family protein SLC25A3 transports both copper and phosphate in mammals, yet in the transport of these substrates is partitioned across two paralogs: PIC2 and MIR1. To understand the ancestral state of copper and phosphate transport in mitochondria, we explored the evolutionary relationships of PIC2 and MIR1 orthologs across the eukaryotic tree of life. Phylogenetic analyses revealed that PIC2-like and MIR1-like orthologs are present in all major eukaryotic supergroups, indicating an ancient gene duplication created these paralogs.

COA6 Is Structurally Tuned to Function as a Thiol-Disulfide Oxidoreductase in Copper Delivery to Mitochondrial Cytochrome c Oxidase.

In eukaryotes, cellular respiration is driven by mitochondrial cytochrome c oxidase (CcO), an enzyme complex that requires copper cofactors for its catalytic activity. Insertion of copper into its catalytically active subunits, including COX2, is a complex process that requires metallochaperones and redox proteins including SCO1, SCO2, and COA6, a recently discovered protein whose molecular function is unknown. To uncover the molecular mechanism by which COA6 and SCO proteins mediate copper delivery to COX2, we have solved the solution structure of COA6, which reveals a coiled-coil-helix-coiled-coil-helix domain typical of redox-active proteins found in the mitochondrial inter-membrane space.

A Microglia Sublineage Protects from Sex-Linked Anxiety Symptoms and Obsessive Compulsion.

Aberrant microglia activity is associated with many neurological and psychiatric disorders, yet our knowledge about the pathological mechanisms is incomplete. Here, we describe a genetically defined microglia sublineage in mice which has the ability to suppress obsessive compulsion and anxiety symptoms. These microglia derive from precursors expressing the transcription factor Hoxb8.

Elesclomol restores mitochondrial function in genetic models of copper deficiency.

Copper is an essential cofactor of cytochrome oxidase (CcO), the terminal enzyme of the mitochondrial respiratory chain. Inherited loss-of-function mutations in several genes encoding proteins required for copper delivery to CcO result in diminished CcO activity and severe pathologic conditions in affected infants. Copper supplementation restores CcO function in patient cells with mutations in two of these genes, and , suggesting a potential therapeutic approach.

Two distinct ontogenies confer heterogeneity to mouse brain microglia.

mutant mice show compulsive behavior similar to trichotillomania, a human obsessive-compulsive-spectrum disorder. The only lineage-labeled cells in the brains of mice are microglia, suggesting that defective microglia caused the disorder. What is the source of the microglia? It has been posited that all microglia progenitors arise at embryonic day (E) 7.

The mammalian phosphate carrier SLC25A3 is a mitochondrial copper transporter required for cytochrome oxidase biogenesis.

Copper is required for the activity of cytochrome oxidase (COX), the terminal electron-accepting complex of the mitochondrial respiratory chain. The likely source of copper used for COX biogenesis is a labile pool found in the mitochondrial matrix. In mammals, the proteins that transport copper across the inner mitochondrial membrane remain unknown.

The mitochondrial metallochaperone SCO1 maintains CTR1 at the plasma membrane to preserve copper homeostasis in the murine heart.

SCO1 is a ubiquitously expressed, mitochondrial protein with essential roles in cytochrome c oxidase (COX) assembly and the regulation of copper homeostasis. SCO1 patients present with severe forms of early onset disease, and ultimately succumb from liver, heart or brain failure. However, the inherent susceptibility of these tissues to SCO1 mutations and the clinical heterogeneity observed across SCO1 pedigrees remain poorly understood phenomena.

The Mitochondrial Metallochaperone SCO1 Is Required to Sustain Expression of the High-Affinity Copper Transporter CTR1 and Preserve Copper Homeostasis.

Human SCO1 fulfills essential roles in cytochrome c oxidase (COX) assembly and the regulation of copper (Cu) homeostasis, yet it remains unclear why pathogenic mutations in this gene cause such clinically heterogeneous forms of disease. Here, we establish a Sco1 mouse model of human disease and show that ablation of Sco1 expression in the liver is lethal owing to severe COX and Cu deficiencies. We further demonstrate that the Cu deficiency is explained by a functional connection between SCO1 and CTR1, the high-affinity transporter that imports Cu into the cell.

Human COX20 cooperates with SCO1 and SCO2 to mature COX2 and promote the assembly of cytochrome c oxidase.

Cytochrome c oxidase (CIV) deficiency is one of the most common respiratory chain defects in patients presenting with mitochondrial encephalocardiomyopathies. CIV biogenesis is complicated by the dual genetic origin of its structural subunits, and assembly of a functional holoenzyme complex requires a large number of nucleus-encoded assembly factors. In general, the functions of these assembly factors remain poorly understood, and mechanistic investigations of human CIV biogenesis have been limited by the availability of model cell lines.

Signaling by FGF4 and FGF8 is required for axial elongation of the mouse embryo.

Fibroblast growth factor (FGF) signaling has been shown to play critical roles in vertebrate segmentation and elongation of the embryonic axis. Neither the exact roles of FGF signaling, nor the identity of the FGF ligands involved in these processes, has been conclusively determined. Fgf8 is required for cell migration away from the primitive streak when gastrulation initiates, but previous studies have shown that drastically reducing the level of FGF8 later in gastrulation has no apparent effect on somitogenesis or elongation of the embryo.

Automatic sample production by depositing solutions on filters for the organization of proficiency tests.

This article describes a device intended to produce replicas on filters by liquid deposition of anion or metal solutions. Schematically, the filters are housed in cassettes labelled automatically by means of a code. An automatic arm takes each cassette, reads the code, and deposits the amount of element required.

Structural basis for recruitment of Rab6-interacting protein 1 to Golgi via a RUN domain.

Small GTPase Rab6 regulates vesicle trafficking at the level of Golgi via recruitment of numerous and unrelated effectors. The crystal structure of Rab6a(GTP) in complex with a 378-residue internal fragment of the effector Rab6IP1 was solved at 3.2 angstroms resolution.

ALASCA proficiency testing scheme for occupational hygiene laboratories.

Nowadays, quality assurance is an important part in the environment of analytical laboratories, who need to prove their ability to perform analysis as well to handle routine control as research and development analysis. A proficiency testing scheme (PTS) is one of the possible and powerful tools to evaluate both bias and dispersion of the analysis. As far as industrial hygiene is concerned, since analytical uncertainty is insignificant with regard to sampling strategy uncertainty, laboratories could be tempted to neglect analytical uncertainty assessment as well.

Rab6-interacting protein 1 links Rab6 and Rab11 function.

Rab11 and Rab6 guanosine triphosphatases are associated with membranes of the recycling endosomes (REs) and Golgi complex, respectively. Evidence indicates that they sequentially regulate a retrograde transport pathway between these two compartments, suggesting the existence of proteins that must co-ordinate their functions. Here, we report the characterization of two isoforms of a protein, Rab6-interacting protein 1 (R6IP1), originally identified as a Rab6-binding protein.

Effect of glycoamphiphiles on the solubilization and dendritic cell uptake of a lipopeptide: a preliminary study.

The selective delivery of antigens to professional antigen-presenting cells represents a promising approach to improve vaccine efficacy. Addition of a glycoamphiphile to a lipopeptide, whose interest for vaccination is now well-established, greatly favors its solubilization in aqueous solutions through the formation of mixed vesicles. Flow cytometry experiments indicate that this formulation does not diminish the uptake of the lipopeptide by the dendritic cells (DCs).

The roles of Fgf4 and Fgf8 in limb bud initiation and outgrowth.

Although numerous molecules required for limb bud formation have recently been identified, the molecular pathways that initiate this process and ensure that limb formation occurs at specific axial positions have yet to be fully elucidated. Based on experiments in the chick, Fgf8 expression in the intermediate mesoderm (IM) has been proposed to play a critical role in the initiation of limb bud outgrowth via restriction of Fgf10 expression to the appropriate region of the lateral plate mesoderm. Contrary to the outcome predicted by this model, ablation of Fgf8 expression in the intermediate mesoderm before limb bud initiation had no effect on initial limb bud outgrowth or on the formation of normal limbs.

Multiple roles of Hoxa11 and Hoxd11 in the formation of the mammalian forelimb zeugopod.

Mutations in the 5' or posterior murine Hox genes (paralogous groups 9-13) markedly affect the formation of the stylopod, zeugopod and autopod of both forelimbs and hindlimbs. Targeted disruption of Hoxa11 and Hoxd11 or Hoxa10, Hoxc10 and Hoxd10 result in gross mispatterning of the radius and ulna or the femur, respectively. Similarly, in mice with disruptions of both Hoxa13 and Hoxd13, development of the forelimb and hindlimb autopod is severely curtailed.