@article{893,
  abstract     = {Amino acid composition of proteins varies substantially between taxa and, thus, can evolve. For example, proteins from organisms with (G+C)-rich (or (A+T)-rich) genomes contain more (or fewer) amino acids encoded by (G+C)-rich codons. However, no universal trends in ongoing changes of amino acid frequencies have been reported. We compared sets of orthologous proteins encoded by triplets of closely related genomes from 15 taxa representing all three domains of life (Bacteria, Archaea and Eukaryota), and used phylogenies to polarize amino acid substitutions. Cys, Met, His, Ser and Phe accrue in at least 14 taxa, whereas Pro, Ala, Glu and Gly are consistently lost. The same nine amino acids are currently accrued or lost in human proteins, as shown by analysis of non-synonymous single-nucleotide polymorphisms. All amino acids with declining frequencies are thought to be among the first incorporated into the genetic code; conversely, all amino acids with increasing frequencies, except Ser, were probably recruited late. Thus, expansion of initially under-represented amino acids, which began over 3,400 million years ago, apparently continues to this day.},
  author       = {Jordan, Ingo and Kondrashov, Fyodor and Adzhubeǐ, Ivan and Wolf, Yuri and Koonin, Eugene and Kondrashov, Alexey and Sunyaev, Shamil},
  issn         = {1476-4687},
  journal      = {Nature},
  number       = {7026},
  pages        = {633 -- 638},
  publisher    = {Nature Publishing Group},
  title        = {{A universal trend of amino acid gain and loss in protein evolution}},
  doi          = {10.1038/nature03306},
  volume       = {433},
  year         = {2005},
}

@article{3809,
  abstract     = {Neural stem cells in various regions of the vertebrate brain continuously generate neurons throughout life. In the mammalian hippocampus, a region important for spatial and episodic memory, thousands of new granule cells are produced per day, with the exact number depending on environmental conditions and physical exercise. The survival of these neurons is improved by learning and conversely learning may be promoted by neurogenesis. Although it has been suggested that newly generated neurons may have specific properties to facilitate learning, the cellular and synaptic mechanisms of plasticity in these neurons are largely unknown. Here we show that young granule cells in the adult hippocampus differ substantially from mature granule cells in both active and passive membrane properties. In young neurons, T-type Ca2+ channels can generate isolated Ca2+ spikes and boost fast Na+ action potentials, contributing to the induction of synaptic plasticity. Associative long-term potentiation can be induced more easily in young neurons than in mature neurons under identical conditions. Thus, newly generated neurons express unique mechanisms to facilitate synaptic plasticity, which may be important for the formation of new memories.},
  author       = {Schmidt Hieber, Christoph and Jonas, Peter M and Bischofberger, Josef},
  issn         = {1476-4687},
  journal      = {Nature},
  number       = {6988},
  pages        = {184 -- 7},
  publisher    = {Nature Publishing Group},
  title        = {{Enhanced synaptic plasticity in newly generated granule cells of the adult hippocampus}},
  doi          = {10.1038/nature02553},
  volume       = {429},
  year         = {2004},
}

@article{898,
  abstract     = {New alleles become fixed owing to random drift of nearly neutral mutations or to positive selection of substantially advantageous mutations. After decades of debate, the fraction of fixations driven by selection remains uncertain. Within 9,390 genes, we analysed 28,196 codons at which rat and mouse differ from each other at two nucleotide sites and 1,982 codons with three differences. At codons where rat-mouse divergence involved two non-synonymous substitutions, both of them occurred in the same lineage, either rat or mouse, in 64% of cases; however, independent substitutions would occur in the same lineage with a probability of only 50%. All three non-synonymous substitutions occurred in the same lineage for 46% of codons, instead of the 25% expected. Furthermore, comparison of 12 pairs of prokaryotic genomes also shows clumping of multiple non-synonymous substitutions in the same lineage. This pattern cannot be explained by correlated mutation or episodes of relaxed negative selection, but instead indicates that positive selection acts at many sites of rapid, successive amino acid replacement.},
  author       = {Bazykin, Georgii and Kondrashov, Fyodor and Ogurtsov, Aleksey and Sunyaev, Shamil and Kondrashov, Alexey},
  issn         = {1476-4687},
  journal      = {Nature},
  number       = {6991},
  pages        = {558 -- 562},
  publisher    = {Nature Publishing Group},
  title        = {{Positive selection at sites of multiple amino acid replacements since rat-mouse divergence}},
  doi          = {10.1038/nature02601},
  volume       = {429},
  year         = {2004},
}

@article{11121,
  abstract     = {In metazoa, the nuclear envelope breaks down and reforms during each cell cycle. Nuclear pore complexes (NPCs), which serve as channels for transport between the nucleus and cytoplasm1, assemble into the reforming nuclear envelope in a sequential process involving association of a subset of NPC proteins, nucleoporins, with chromatin followed by the formation of a closed nuclear envelope fenestrated by NPCs2,3,4,5,6,7. How chromatin recruitment of nucleoporins and NPC assembly are regulated is unknown. Here we demonstrate that RanGTP production is required to dissociate nucleoporins Nup107, Nup153 and Nup358 from Importin β, to target them to chromatin and to induce association between separate NPC subcomplexes. Additionally, either an excess of RanGTP or removal of Importin β induces formation of NPC-containing membrane structures—annulate lamellae—both in vitro in the absence of chromatin and in vivo. Annulate lamellae formation is strongly and specifically inhibited by an excess of Importin β. The data demonstrate that RanGTP triggers distinct steps of NPC assembly, and suggest a mechanism for the spatial restriction of NPC assembly to the surface of chromatin.},
  author       = {Walther, Tobias C. and Askjaer, Peter and Gentzel, Marc and Habermann, Anja and Griffiths, Gareth and Wilm, Matthias and Mattaj, Iain W. and HETZER, Martin W},
  issn         = {1476-4687},
  journal      = {Nature},
  keywords     = {Multidisciplinary},
  number       = {6949},
  pages        = {689--694},
  publisher    = {Springer Nature},
  title        = {{RanGTP mediates nuclear pore complex assembly}},
  doi          = {10.1038/nature01898},
  volume       = {424},
  year         = {2003},
}

@article{2994,
  abstract     = {The regular arrangement of leaves around a plant's stem, called phyllotaxis, has for centuries attracted the attention of philosophers, mathematicians and natural scientists; however, to date, studies of phyllotaxis have been largely theoretical. Leaves and flowers are formed from the shoot apical meristem, triggered by the plant hormone auxin. Auxin is transported through plant tissues by specific cellular influx and efflux carrier proteins. Here we show that proteins involved in auxin transport regulate phyllotaxis. Our data indicate that auxin is transported upwards into the meristem through the epidermis and the outermost meristem cell layer. Existing leaf primordia act as sinks, redistributing auxin and creating its heterogeneous distribution in the meristem. Auxin accumulation occurs only at certain minimal distances from existing primordia, defining the position of future primordia. This model for phyllotaxis accounts for its reiterative nature, as well as its regularity and stability.},
  author       = {Reinhardt, Didier and Pesce, Eva and Stieger, Pia and Mandel, Therese and Baltensperger, Kurt and Bennett, Malcolm and Traas, Jan and Friml, Jirí and Kuhlemeier, Cris},
  issn         = {1476-4687},
  journal      = {Nature},
  pages        = {255 -- 260},
  publisher    = {Springer Nature},
  title        = {{Regulation of phyllotaxis by polar auxin transport}},
  doi          = {10.1038/nature02081},
  volume       = {426},
  year         = {2003},
}

@article{2995,
  abstract     = {Axis formation occurs in plants, as in animals, during early embryogenesis. However, the underlying mechanism is not known. Here we show that the first manifestation of the apical-basal axis in plants, the asymmetric division of the zygote, produces a basal cell that transports and an apical cell that responds to the signalling molecule auxin. This apical-basal auxin activity gradient triggers the specification of apical embryo structures and is actively maintained by a novel component of auxin efflux, PIN7, which is located apically in the basal cell. Later, the developmentally regulated reversal of PIN7 and onset of PIN1 polar localization reorganize the auxin gradient for specification of the basal root pole. An analysis of pin quadruple mutants identifies PIN-dependent transport as an essential part of the mechanism for embryo axis formation. Our results indicate how the establishment of cell polarity, polar auxin efflux and local auxin response result in apical-basal axis formation of the embryo, and thus determine the axiality of the adult plant.
},
  author       = {Friml, Jirí and Vieten, Anne and Sauer, Michael and Weijers, Dolf and Schwarz, Heinz and Hamann, Thorsten and Offringa, Remko and Jürgens, Gerd},
  issn         = {1476-4687},
  journal      = {Nature},
  pages        = {147 -- 153},
  publisher    = {Springer Nature},
  title        = {{Efflux dependent auxin gradients establish the apical basal axis of Arabidopsis}},
  doi          = {10.1038/nature02085},
  volume       = {426},
  year         = {2003},
}

@article{2482,
  abstract     = {The complementary DNA of a metabotropic glutamate receptor coupled to inositol phosphate/Ca2+ signal transduction has been cloned and characterized. This receptor shows no sequence similarity to conventional G protein-coupled receptors and has a unique structure with large hydrophilic sequences at both sides of seven putative membrane-spanning domains. Abundant expression of this messenger RNA is observed in neuronal cells in hippocampal dentate gyrus and CA2-3 and in cerebellar Purkinje cells, suggesting the importance of this receptor in specific hippocampal and cerebellar functions.},
  author       = {Masu, Masayuki and Tanabe, Yasuto and Tsuchida, Kunihiro and Shigemoto, Ryuichi and Nakanishi, Shigetada},
  issn         = {1476-4687},
  journal      = {Nature},
  number       = {6312},
  pages        = {760 -- 765},
  publisher    = {Nature Publishing Group},
  title        = {{Sequence and expression of a metabotropic glutamate receptor}},
  doi          = {10.1038/349760a0},
  volume       = {349},
  year         = {1991},
}

@article{2483,
  abstract     = {A complementary DNA encoding the rat NMDA receptor has been cloned and characterized. The single protein encoded by the cDNA forms a receptor-channel complex that has electrophysiological and pharmacological properties characteristic of the NMDA receptor. This protein has a significant sequence similarity to the AMPA/kainate receptors and contains four putative transmembrane segments following a large extracellular domain. The NMDA receptor messenger RNA is expressed in neuronal cells throughout the brain regions, particularly in the hippocampus, cerebral cortex and cerebellum.},
  author       = {Moriyoshi, Koki and Masu, Masayuki and Ishii, Takahiro and Shigemoto, Ryuichi and Mizuno, Noboru and Nakanishi, Shigetada},
  issn         = {1476-4687},
  journal      = {Nature},
  number       = {6348},
  pages        = {31 -- 37},
  publisher    = {Nature Publishing Group},
  title        = {{Molecular cloning and characterization of the rat NMDA receptor}},
  doi          = {10.1038/354031a0},
  volume       = {353},
  year         = {1991},
}

@article{4310,
  author       = {Barton, Nicholas H and Jones, Steve},
  issn         = {1476-4687},
  journal      = {Nature},
  pages        = {415 -- 416},
  publisher    = {Nature Publishing Group},
  title        = {{The language of the genes}},
  doi          = {10.1038/346415a0},
  volume       = {346},
  year         = {1990},
}

@article{3654,
  abstract     = {Many species are divided into a mosaic of genetically distinct populations, separated by narrow zones of hybridization. Studies of hybrid zones allow us to quantify the genetic differences responsible for speciation, to measure the diffusion of genes between diverging taxa, and to understand the spread of alternative adaptations.},
  author       = {Barton, Nicholas H and Hewitt, Godfrey},
  issn         = {1476-4687},
  journal      = {Nature},
  pages        = {497 -- 503},
  publisher    = {Nature Publishing Group},
  title        = {{Adaptation, speciation and hybrid zones}},
  doi          = {10.1038/341497a0},
  volume       = {341},
  year         = {1989},
}

@misc{4315,
  author       = {Coyne, Jerry and Barton, Nicholas H},
  booktitle    = {Nature},
  issn         = {1476-4687},
  pages        = {485 -- 486},
  publisher    = {Nature Publishing Group},
  title        = {{What do we know about speciation?}},
  doi          = {10.1038/331485a0},
  volume       = {331},
  year         = {1988},
}

@misc{4316,
  author       = {Barton, Nicholas H and Jones, Steve},
  booktitle    = {Nature},
  issn         = {1476-4687},
  pages        = {597 -- 597},
  publisher    = {Springer Nature},
  title        = {{Molecular evolutionary genetics}},
  doi          = {10.1038/332597a0},
  volume       = {332},
  year         = {1988},
}

@misc{4318,
  author       = {Barton, Nicholas H and Jones, Steve and Mallet, James},
  booktitle    = {Nature},
  issn         = {1476-4687},
  pages        = {13 -- 14},
  publisher    = {Springer Nature},
  title        = {{No barriers to speciation}},
  doi          = {10.1038/336013a0},
  volume       = {336},
  year         = {1988},
}

@article{3598,
  author       = {Barton, Nicholas H and Jones, Steve},
  issn         = {1476-4687},
  journal      = {Nature},
  pages        = {317 -- 318},
  publisher    = {Springer Nature},
  title        = {{Mitochondrial DNA: new clues about evolution}},
  doi          = {10.1038/306317a0},
  volume       = {306},
  year         = {1983},
}

