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1 Ultralow-loading platinum-cobalt fuel cell catalysts derived from imidazolate frameworks 2018-11-10             

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Achieving high catalytic performance with the lowest amount of platinum is critical in fuel cell cost reduction. We describe a method of preparing highly active yet stable electrocatalysts containing ultralow Pt content using Co or Co/Zn zeolitic imidazolate frameworks as precursors. Synergistic catalysis between strained Pt-Co core-shell nanoparticles over a platinum-group-metal-free (PGM-free) catalytic substrate led to excellent fuel cell performance under 1 atmosphere of O2 or air at both high voltage and high current domains. Two catalysts achieved the oxygen reduction reaction (ORR) mass activities of 1.08 A mgPt–1/1.77 A mgPt–1 and retained 64%/15% of initial values after 30,000 voltage cycles in fuel cell. Computational modeling reveals that the interaction between Pt-Co and PGM-free sites improves ORR activity and durability.

2 Quantifying the contribution of recessive coding variation to developmental disorders 2018-11-10             

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We estimated the genome-wide contribution of recessive coding variation from 6,040 families from the Deciphering Developmental Disorders study. The proportion of cases attributable to recessive coding variants was 3.6% in patients of European ancestry, compared to 50% explained by de novo coding mutations. It was higher (31%) in patients with Pakistani ancestry, due to elevated autozygosity. Half of this recessive burden is attributable to known genes. We identified two genes not previously associated with recessive developmental disorders, KDM5B and EIF3F, and functionally validated them with mouse and cellular models. Our results suggest that recessive coding variants account for a small fraction of currently undiagnosed non-consanguineous individuals, and that the role of noncoding variants, incomplete penetrance, and polygenic mechanisms need further exploration.

3 Formyl-methionine as an N-degron of a eukaryotic N-end rule pathway 2018-11-10             

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In bacteria, nascent proteins bear the pretranslationally generated N-terminal (Nt) formyl-methionine (fMet) residue. Nt-fMet of bacterial proteins is a degradation signal, termed fMet/N-degron. In contrast, proteins synthesized by cytosolic ribosomes of eukaryotes were presumed to bear unformylated Nt-Met. Here we found that the yeast formyltransferase Fmt1, although imported into mitochondria, could also produce Nt-formylated proteins in the cytosol. Nt-formylated proteins were strongly up-regulated in stationary phase or upon starvation for specific amino acids. This up-regulation strictly required the Gcn2 kinase, which phosphorylates Fmt1 and mediates its retention in the cytosol. We also found that the Nt-fMet residues of Nt-formylated proteins act as fMet/N-degrons, and identified the Psh1 ubiquitin ligase as the recognition component of this eukaryotic fMet/N-end rule pathway, which destroys Nt-formylated proteins.

4 Early human dispersals within the Americas 2018-11-10             

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Studies of the peopling of the Americas have focused on the timing and number of initial migrations. Less attention has been paid to the subsequent spread of people within the Americas. We sequenced 15 ancient human genomes spanning Alaska to Patagonia; six are ≥10,000 years old (up to ~18x coverage). All are most closely related to Native Americans, including an Ancient Beringian individual, and two morphologically distinct "Paleoamericans." We find evidence of rapid dispersal and early diversification, including previously unknown groups, as people moved south. This resulted in multiple independent, geographically uneven migrations, including one that provides clues of a Late Pleistocene Australasian genetic signal, and a later Mesoamerican-related expansion. These led to complex and dynamic population histories from North to South America.

5 Quantifying reputation and success in art 2018-11-10             

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In areas of human activity where performance is difficult to quantify in an objective fashion, reputation and networks of influence play a key role in determining access to resources and rewards. To understand the role of these factors, we reconstructed the exhibition history of half a million artists, mapping out the coexhibition network that captures the movement of art between institutions. Centrality within this network captured institutional prestige, allowing us to explore the career trajectory of individual artists in terms of access to coveted institutions. Early access to prestigious central institutions offered life-long access to high-prestige venues and reduced dropout rate. By contrast, starting at the network periphery resulted in a high dropout rate, limiting access to central institutions. A Markov model predicts the career trajectory of individual artists and documents the strong path and history dependence of valuation in art.

6 E-C coupling structural protein junctophilin-2 encodes a stress-adaptive transcription regulator 2018-11-10             

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Junctophilin-2 (JP2) is a structural protein required for normal excitation-contraction (E-C) coupling. Following cardiac stress, JP2 is cleaved by Ca2+-dependent protease calpain, which disrupts the E-C coupling ultrastructural machinery and drives heart failure progression. Here we demonstrate that stress-induced proteolysis of JP2 liberates an N-terminal fragment (JP2NT) that translocates to the nucleus, binds to genomic DNA and controls expression of a spectrum of genes in cardiomyocytes. Transgenic overexpression of JP2NT in mice modifies the transcriptional profile resulting in attenuated pathological remodeling in response to cardiac stress. Conversely, loss of JP2NT function accelerates stress-induced development of hypertrophy and heart failure in mutant mice. These data reveal a self-protective mechanism in failing cardiomyocytes that transduce mechanical information (E-C uncoupling) into salutary transcriptional reprogramming in the stressed heart.

7 Human tumor genomics and zebrafish modeling identify SPRED1 loss as a driver of mucosal melanoma 2018-11-03             

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Melanomas originating from mucosal surfaces have low mutation burden, genomic instability, and poor prognosis. To identify potential driver genes, we sequenced hundreds of cancer-related genes in 43 human mucosal melanomas, cataloguing point mutations, amplifications and deletions. The SPRED1 gene, which encodes a negative regulator of MAPK signaling, was inactivated in 37% of the tumors. Four distinct genotypes were associated with SPRED1 loss. Using a rapid, tissue-specific CRISPR technique to model these genotypes in zebrafish, we found that SPRED1 functions as a tumor suppressor, particularly in the context of KIT mutations. SPRED1 knockdown caused MAPK activation, increased cell proliferation and conferred resistance to drugs inhibiting KIT tyrosine kinase activity. These findings provide a rationale for MAPK inhibition in SPRED1-deficient melanomas and introduce a zebrafish modeling approach that can be used more generally to dissect genetic interactions in cancer.

8 Molecular, spatial and functional single-cell profiling of the hypothalamic preoptic region 2018-11-03             

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The hypothalamus controls essential social behaviors and homeostatic functions. However, the cellular architecture of hypothalamic nuclei, including the molecular identity, spatial organization, and function of distinct cell types, is poorly understood. Here, we developed an imaging-based in situ cell type identification and mapping method and combined it with single-cell RNA-sequencing to create a molecularly annotated and spatially resolved cell atlas of the mouse hypothalamic preoptic region. We profiled ~1 million cells, identified ~70 neuronal populations characterized by distinct neuromodulatory signatures and spatial organizations, and defined specific neuronal populations activated during social behaviors in male and female mice, providing a high-resolution framework for mechanistic investigation of behavior circuits. The approach described opens a new avenue for the construction of cell atlases in diverse tissues and organisms.

9 A Nobel opportunity for interdisciplinarity 2018-11-02             

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A Nobel opportunity for interdisciplinarity

A Nobel opportunity for interdisciplinarity, Published online: 01 November 2018; doi:10.1038/s41567-018-0314-6

Despite the growing interdisciplinarity of research, the Nobel prize consolidates the traditional disciplinary categorization of science. There is, in fact, an opportunity for the most revered scientific reward to mirror the current research landscape.

10 Confused at a higher level 2018-11-02             

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Confused at a higher level

Confused at a higher level, Published online: 01 November 2018; doi:10.1038/s41567-018-0333-3

Confused at a higher level

 
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