@article{12187, abstract = {Genomes of germ cells present an existential vulnerability to organisms because germ cell mutations will propagate to future generations. Transposable elements are one source of such mutations. In the small flowering plant Arabidopsis, Long et al. found that genome methylation in the male germline is directed by small interfering RNAs (siRNAs) imperfectly transcribed from transposons (see the Perspective by Mosher). These germline siRNAs silence germline transposons and establish inherited methylation patterns in sperm, thus maintaining the integrity of the plant genome across generations.}, author = {Long, Jincheng and Walker, James and She, Wenjing and Aldridge, Billy and Gao, Hongbo and Deans, Samuel and Vickers, Martin and Feng, Xiaoqi}, issn = {0036-8075}, journal = {Science}, keywords = {Multidisciplinary}, number = {6550}, publisher = {American Association for the Advancement of Science (AAAS)}, title = {{Nurse cell--derived small RNAs define paternal epigenetic inheritance in Arabidopsis}}, doi = {10.1126/science.abh0556}, volume = {373}, year = {2021}, } @article{7, abstract = {Animal social networks are shaped by multiple selection pressures, including the need to ensure efficient communication and functioning while simultaneously limiting disease transmission. Social animals could potentially further reduce epidemic risk by altering their social networks in the presence of pathogens, yet there is currently no evidence for such pathogen-triggered responses. We tested this hypothesis experimentally in the ant Lasius niger using a combination of automated tracking, controlled pathogen exposure, transmission quantification, and temporally explicit simulations. Pathogen exposure induced behavioral changes in both exposed ants and their nestmates, which helped contain the disease by reinforcing key transmission-inhibitory properties of the colony's contact network. This suggests that social network plasticity in response to pathogens is an effective strategy for mitigating the effects of disease in social groups.}, author = {Stroeymeyt, Nathalie and Grasse, Anna V and Crespi, Alessandro and Mersch, Danielle and Cremer, Sylvia and Keller, Laurent}, issn = {1095-9203}, journal = {Science}, number = {6417}, pages = {941 -- 945}, publisher = {AAAS}, title = {{Social network plasticity decreases disease transmission in a eusocial insect}}, doi = {10.1126/science.aat4793}, volume = {362}, year = {2018}, } @article{7718, abstract = {Flores Island, Indonesia, was inhabited by the small-bodied hominin species Homo floresiensis, which has an unknown evolutionary relationship to modern humans. This island is also home to an extant human pygmy population. Here we describe genome-scale single-nucleotide polymorphism data and whole-genome sequences from a contemporary human pygmy population living on Flores near the cave where H. floresiensis was found. The genomes of Flores pygmies reveal a complex history of admixture with Denisovans and Neanderthals but no evidence for gene flow with other archaic hominins. Modern individuals bear the signatures of recent positive selection encompassing the FADS (fatty acid desaturase) gene cluster, likely related to diet, and polygenic selection acting on standing variation that contributed to their short-stature phenotype. Thus, multiple independent instances of hominin insular dwarfism occurred on Flores.}, author = {Tucci, Serena and Vohr, Samuel H. and McCoy, Rajiv C. and Vernot, Benjamin and Robinson, Matthew Richard and Barbieri, Chiara and Nelson, Brad J. and Fu, Wenqing and Purnomo, Gludhug A. and Sudoyo, Herawati and Eichler, Evan E. and Barbujani, Guido and Visscher, Peter M. and Akey, Joshua M. and Green, Richard E.}, issn = {0036-8075}, journal = {Science}, number = {6401}, pages = {511--516}, publisher = {American Association for the Advancement of Science}, title = {{Evolutionary history and adaptation of a human pygmy population of Flores Island, Indonesia}}, doi = {10.1126/science.aar8486}, volume = {361}, year = {2018}, } @article{7310, abstract = {The rechargeable nonaqueous lithium-air (Li-O2) battery is receiving a great deal of interest because, theoretically, its specific energy far exceeds the best that can be achieved with lithium-ion cells. Operation of the rechargeable Li-O2 battery depends critically on repeated and highly reversible formation/decomposition of lithium peroxide (Li2O2) at the cathode upon cycling. Here, we show that this process is possible with the use of a dimethyl sulfoxide electrolyte and a porous gold electrode (95% capacity retention from cycles 1 to 100), whereas previously only partial Li2O2 formation/decomposition and limited cycling could occur. Furthermore, we present data indicating that the kinetics of Li2O2 oxidation on charge is approximately 10 times faster than on carbon electrodes.}, author = {Peng, Z. and Freunberger, Stefan Alexander and Chen, Y. and Bruce, P. G.}, issn = {0036-8075}, journal = {Science}, number = {6094}, pages = {563--566}, publisher = {AAAS}, title = {{A reversible and higher-rate Li-O2 battery}}, doi = {10.1126/science.1223985}, volume = {337}, year = {2012}, } @article{8074, abstract = {Cortical neurons receive balanced excitatory and inhibitory synaptic currents. Such a balance could be established and maintained in an experience-dependent manner by synaptic plasticity at inhibitory synapses. We show that this mechanism provides an explanation for the sparse firing patterns observed in response to natural stimuli and fits well with a recently observed interaction of excitatory and inhibitory receptive field plasticity. The introduction of inhibitory plasticity in suitable recurrent networks provides a homeostatic mechanism that leads to asynchronous irregular network states. Further, it can accommodate synaptic memories with activity patterns that become indiscernible from the background state but can be reactivated by external stimuli. Our results suggest an essential role of inhibitory plasticity in the formation and maintenance of functional cortical circuitry.}, author = {Vogels, Tim P and Sprekeler, H. and Zenke, F. and Clopath, C. and Gerstner, W.}, issn = {0036-8075}, journal = {Science}, number = {6062}, pages = {1569--1573}, publisher = {American Association for the Advancement of Science}, title = {{Inhibitory plasticity balances excitation and inhibition in sensory pathways and memory networks}}, doi = {10.1126/science.1211095}, volume = {334}, year = {2011}, } @article{11118, abstract = {Nuclear pore complexes are multiprotein channels that span the double lipid bilayer of the nuclear envelope. How new pores are inserted into the intact nuclear envelope of proliferating and differentiating eukaryotic cells is unknown. We found that the Nup107-160 complex was incorporated into assembly sites in the nuclear envelope from both the nucleoplasmic and the cytoplasmic sides. Nuclear pore insertion required the generation of Ran guanosine triphosphate in the nuclear and cytoplasmic compartments. Newly formed nuclear pore complexes did not contain structural components of preexisting pores, suggesting that they can form de novo.}, author = {D'Angelo, Maximiliano A. and Anderson, Daniel J. and Richard, Erin and HETZER, Martin W}, issn = {0036-8075}, journal = {Science}, keywords = {Multidisciplinary}, number = {5772}, pages = {440--443}, publisher = {American Association for the Advancement of Science}, title = {{Nuclear pores form de novo from both sides of the nuclear envelope}}, doi = {10.1126/science.1124196}, volume = {312}, year = {2006}, } @article{7706, abstract = {The Sir2 deacetylase modulates organismal life-span in various species. However, the molecular mechanisms by which Sir2 increases longevity are largely unknown. We show that in mammalian cells, the Sir2 homolog SIRT1 appears to control the cellular response to stress by regulating the FOXO family of Forkhead transcription factors, a family of proteins that function as sensors of the insulin signaling pathway and as regulators of organismal longevity. SIRT1 and the FOXO transcription factor FOXO3 formed a complex in cells in response to oxidative stress, and SIRT1 deacetylated FOXO3 in vitro and within cells. SIRT1 had a dual effect on FOXO3 function: SIRT1 increased FOXO3's ability to induce cell cycle arrest and resistance to oxidative stress but inhibited FOXO3's ability to induce cell death. Thus, one way in which members of the Sir2 family of proteins may increase organismal longevity is by tipping FOXO-dependent responses away from apoptosis and toward stress resistance.}, author = {Brunet, Anne and Sweeney, Lora Beatrice Jaeger and Sturgill, J Fitzhugh and Chua, Katrin and Greer, Paul and Lin, Yingxi and Tran, Hien and Ross, Sarah and Mostoslavsky, Raul and Cohen, Haim and Hu, Linda and Chen, Hwei-Ling and Jedrychowski, Mark and Gygi, Steven and Sinclair, David and Alt, Frederick and Greenberg, Michael}, issn = {0036-8075}, journal = {Science}, number = {5666}, pages = {2011--2015}, publisher = {American Association for the Advancement of Science}, title = {{Stress-dependent regulation of FOXO transcription factors by the SIRT1 deacetylase}}, doi = {10.1126/science.1094637}, volume = {303}, year = {2004}, }