@article{4256,
  abstract     = {Artificial Life models may shed new light on the long-standing challenge for evolutionary biology of explaining the origins of complex organs. Real progress on this issue, however, requires Artificial Life researchers to take seriously the tools and insights from population genetics.},
  author       = {Barton, Nicholas H and Zuidema, Willem},
  issn         = {0960-9822},
  journal      = {Current Biology},
  number       = {16},
  pages        = {R649 -- R651},
  publisher    = {Cell Press},
  title        = {{The erratic path towards complexity}},
  doi          = {10.1016/S0960-9822(03)00573-6},
  volume       = {13},
  year         = {2003},
}

@article{2988,
  abstract     = {Coordination of cell and tissue polarity commonly involves directional signaling [1]. In the Arabidopsis root epidermis, cell polarity is revealed by basal, root tip-oriented, hair outgrowth from hair-forming cells (trichoblasts) [2]. The plant hormone auxin displays polar movements [1, 3] and accumulates at maximum concentration in the root tip [4, 5]. The application of polar auxin transport inhibitors [3] evokes changes in trichoblast polarity only at high concentrations and after long-term application [2, 4]. Thus, it remains open whether components of the auxin transport machinery mediate establishment of trichoblast polarity. Here we report that the presumptive auxin influx carrier AUX1 [6, 7] contributes to apical-basal hair cell polarity. AUX1 function is required for polarity changes induced by exogenous application of the auxin 2,4-D, a preferential influx carrier substrate. Similar to aux1 mutants, the vesicle trafficking inhibitor brefeldin A (BFA) interferes with polar hair initiation, and AUX1 function is required for BFA-mediated polarity changes. Consistently, BFA inhibits membrane trafficking of AUX1, trichoblast hyperpolarization induced by 2,4-D, and alters the distal auxin maximum. Our results identify AUX1 as one component of a novel BFA-sensitive auxin transport pathway polarizing cells toward a hormone maximum.},
  author       = {Grebe, Markus and Friml, Jirí and Swarup, Ranjan and Ljung, Karin and Sandberg, Göran and Terlou, Maarten and Palme, Klaus and Bennett, Malcolm and Scheres, Ben},
  issn         = {0960-9822},
  journal      = {Current Biology},
  number       = {4},
  pages        = {329 -- 334},
  publisher    = {Cell Press},
  title        = {{Cell polarity signaling in Arabidopsis involves a BFA sensitive auxin influx pathway}},
  doi          = {10.1016/S0960-9822(02)00654-1},
  volume       = {12},
  year         = {2002},
}

@article{11124,
  abstract     = {Ran GTPase plays important roles in nucleocytoplasmic transport in interphase [1, 2] and in both spindle formation and nuclear envelope (NE) assembly during mitosis [3, 4, 5]. The latter functions rely on the presence of high local concentrations of GTP-bound Ran near mitotic chromatin [3, 4, 5]. RanGTP localization has been proposed to result from the association of Ran's GDP/GTP exchange factor, RCC1, with chromatin [6, 7, 8, 9], but Ran is shown here to bind directly to chromatin in two modes, either dependent or independent of RCC1, and, where bound, to increase the affinity of chromatin for NE membranes. We propose that the Ran binding capacity of chromatin contributes to localized spindle and NE assembly.},
  author       = {Bilbao-Cortés, Daniel and HETZER, Martin W and Längst, Gernot and Becker, Peter B. and Mattaj, Iain W.},
  issn         = {0960-9822},
  journal      = {Current Biology},
  keywords     = {General Agricultural and Biological Sciences, General Biochemistry, Genetics and Molecular Biology},
  number       = {13},
  pages        = {1151--1156},
  publisher    = {Elsevier BV},
  title        = {{Ran binds to chromatin by two distinct mechanisms}},
  doi          = {10.1016/s0960-9822(02)00927-2},
  volume       = {12},
  year         = {2002},
}

@article{4199,
  abstract     = {Recent studies on vertebrate homologues of the van gogh/strabismus (vang/stbm) gene, a key player in planar cell polarity signalling in Drosophila, show that vang/stbm is involved in patterning and morphogenesis during vertebrate gastrulation where it modulates two distinct Wnt signals.},
  author       = {Heisenberg, Carl-Philipp J and Tada, Masazumi},
  issn         = {0960-9822},
  journal      = {Current Biology},
  number       = {4},
  pages        = {R126 -- R128},
  publisher    = {Cell Press},
  title        = {{Wnt signalling: A moving picture emerges from van gogh}},
  doi          = {10.1016/S0960-9822(02)00704-2},
  volume       = {12},
  year         = {2002},
}

@article{4207,
  abstract     = {Vertebrate homologues of the Strabismus/van Gogh (stbm/vang) gene have been implicated in patterning and morphogenesis during gastrulation. Recent work shows that stbm/vang is mutated in zebrafish trilobite mutants and that stbm/vang is required for morphogenesis but not patterning during zebrafish gastrulation.},
  author       = {Heisenberg, Carl-Philipp J},
  issn         = {0960-9822},
  journal      = {Current Biology},
  number       = {19},
  pages        = {R657 -- R659},
  publisher    = {Cell Press},
  title        = {{Wnt signalling: Refocusing on Strabismus}},
  doi          = {10.1016/S0960-9822(02)01160-0},
  volume       = {12},
  year         = {2002},
}

@article{4289,
  abstract     = {A worldwide survey of polymorphic molecular markers shows that the human population is genetically homogeneous, in close agreement with evidence from quite different genes and traits.},
  author       = {Barton, Nicholas H},
  issn         = {0960-9822},
  journal      = {Current Biology},
  number       = {12},
  pages        = {757 -- 758},
  publisher    = {Cell Press},
  title        = {{Population genetics: A new apportionment of human diversity}},
  doi          = {10.1016/S0960-9822(06)00397-6},
  volume       = {7},
  year         = {1997},
}

@inbook{4295,
  abstract     = {Genetic studies are beginning to provide insights into the evolutionary processes that reduce the fitness of hybrids between recently diverged species. However, the deleterious gene interactions responsible for this fitness reduction are still poorly understood.},
  author       = {Barton, Nicholas H},
  booktitle    = {Current Biology},
  issn         = {0960-9822},
  pages        = {1244 -- 1246},
  publisher    = {Cell Press},
  title        = {{Speciation: more than the sum of its parts}},
  doi          = {10.1016/S0960-9822(02)70707-0},
  volume       = {6},
  year         = {1996},
}

@article{4304,
  author       = {Barton, Nicholas H},
  issn         = {0960-9822},
  journal      = {Current Biology},
  number       = {11},
  pages        = {797 -- 799},
  publisher    = {Cell Press},
  title        = {{Why species and subspecies?}},
  doi          = {10.1016/0960-9822(93)90036-N},
  volume       = {3},
  year         = {1993},
}

