@article{9491, abstract = {Cytosine DNA methylation in vertebrates is widespread, but methylation in plants is found almost exclusively at transposable elements and repetitive DNA [1]. Within regions of methylation, methylcytosines are typically found in CG, CNG, and asymmetric contexts. CG sites are maintained by a plant homolog of mammalian Dnmt1 acting on hemi-methylated DNA after replication. Methylation of CNG and asymmetric sites appears to be maintained at each cell cycle by other mechanisms. We report a new type of DNA methylation in Arabidopsis, dense CG methylation clusters found at scattered sites throughout the genome. These clusters lack non-CG methylation and are preferentially found in genes, although they are relatively deficient toward the 5′ end. CG methylation clusters are present in lines derived from different accessions and in mutants that eliminate de novo methylation, indicating that CG methylation clusters are stably maintained at specific sites. Because 5-methylcytosine is mutagenic, the appearance of CG methylation clusters over evolutionary time predicts a genome-wide deficiency of CG dinucleotides and an excess of C(A/T)G trinucleotides within transcribed regions. This is exactly what we find, implying that CG methylation clusters have contributed profoundly to plant gene evolution. We suggest that CG methylation clusters silence cryptic promoters that arise sporadically within transcription units.}, author = {Tran, Robert K. and Henikoff, Jorja G. and Zilberman, Daniel and Ditt, Renata F. and Jacobsen, Steven E. and Henikoff, Steven}, issn = {1879-0445}, journal = {Current Biology}, number = {2}, pages = {154--159}, publisher = {Elsevier}, title = {{DNA methylation profiling identifies CG methylation clusters in Arabidopsis genes}}, doi = {10.1016/j.cub.2005.01.008}, volume = {15}, year = {2005}, } @article{6154, author = {Cheung, Benny H.H. and Cohen, Merav and Rogers, Candida and Albayram, Onder and de Bono, Mario}, issn = {0960-9822}, journal = {Current Biology}, number = {10}, pages = {905--917}, publisher = {Elsevier}, title = {{Experience-dependent modulation of C. elegans behavior by ambient oxygen}}, doi = {10.1016/j.cub.2005.04.017}, volume = {15}, year = {2005}, } @article{9493, abstract = {In a number of organisms, transgenes containing transcribed inverted repeats (IRs) that produce hairpin RNA can trigger RNA-mediated silencing, which is associated with 21-24 nucleotide small interfering RNAs (siRNAs). In plants, IR-driven RNA silencing also causes extensive cytosine methylation of homologous DNA in both the transgene "trigger" and any other homologous DNA sequences--"targets". Endogenous genomic sequences, including transposable elements and repeated elements, are also subject to RNA-mediated silencing. The RNA silencing gene ARGONAUTE4 (AGO4) is required for maintenance of DNA methylation at several endogenous loci and for the establishment of methylation at the FWA gene. Here, we show that mutation of AGO4 substantially reduces the maintenance of DNA methylation triggered by IR transgenes, but AGO4 loss-of-function does not block the initiation of DNA methylation by IRs. AGO4 primarily affects non-CG methylation of the target sequences, while the IR trigger sequences lose methylation in all sequence contexts. Finally, we find that AGO4 and the DRM methyltransferase genes are required for maintenance of siRNAs at a subset of endogenous sequences, but AGO4 is not required for the accumulation of IR-induced siRNAs or a number of endogenous siRNAs, suggesting that AGO4 may function downstream of siRNA production.}, author = {Zilberman, Daniel and Cao, Xiaofeng and Johansen, Lisa K. and Xie, Zhixin and Carrington, James C. and Jacobsen, Steven E.}, issn = {1879-0445}, journal = {Current Biology}, number = {13}, pages = {1214--1220}, publisher = {Elsevier}, title = {{Role of Arabidopsis ARGONAUTE4 in RNA-directed DNA methylation triggered by inverted repeats}}, doi = {10.1016/j.cub.2004.06.055}, volume = {14}, year = {2004}, } @article{6155, abstract = {The genome of the nematode Caenorhabditis elegans encodes seven soluble guanylate cyclases (sGCs) [1]. In mammals, sGCs function as α/β heterodimers activated by gaseous ligands binding to a haem prosthetic group 2, 3. The principal activator is nitric oxide, which acts through sGCs to regulate diverse cellular events. In C. elegans the function of sGCs is mysterious: the worm genome does not appear to encode nitric oxide synthase, and all C. elegans sGC subunits are more closely related to mammalian β than α subunits [1]. Here, we show that two of the seven C. elegans sGCs, GCY-35 and GCY-36, promote aggregation behavior. gcy-35 and gcy-36 are expressed in a small number of neurons. These include the body cavity neurons AQR, PQR, and URX, which are directly exposed to the blood equivalent of C. elegans and regulate aggregation behavior [4]. We show that GCY-35 and GCY-36 act as α-like and β-like sGC subunits and that their function in the URX sensory neurons is sufficient for strong nematode aggregation. Neither GCY-35 nor GCY-36 is absolutely required for C. elegans to aggregate. Instead, these molecules may transduce one of several pathways that induce C. elegans to aggregate or may modulate aggregation by responding to cues in C. elegans body fluid.}, author = {Cheung, Benny H.H and Arellano-Carbajal, Fausto and Rybicki, Irene and de Bono, Mario}, issn = {0960-9822}, journal = {Current Biology}, number = {12}, pages = {1105--1111}, publisher = {Elsevier}, title = {{Soluble guanylate cyclases act in neurons exposed to the body fluid to promote C. elegans aggregation behavior}}, doi = {10.1016/j.cub.2004.06.027}, volume = {14}, year = {2004}, } @article{9495, abstract = {RNA interference is a conserved process in which double-stranded RNA is processed into 21–25 nucleotide siRNAs that trigger posttranscriptional gene silencing. In addition, plants display a phenomenon termed RNA-directed DNA methylation (RdDM) in which DNA with sequence identity to silenced RNA is de novo methylated at its cytosine residues. This methylation is not only at canonical CpG sites but also at cytosines in CpNpG and asymmetric sequence contexts. In this report, we study the role of the DRM and CMT3 DNA methyltransferase genes in the initiation and maintenance of RdDM. Neither drm nor cmt3 mutants affected the maintenance of preestablished RNA-directed CpG methylation. However, drm mutants showed a nearly complete loss of asymmetric methylation and a partial loss of CpNpG methylation. The remaining asymmetric and CpNpG methylation was dependent on the activity of CMT3, showing that DRM and CMT3 act redundantly to maintain non-CpG methylation. These DNA methyltransferases appear to act downstream of siRNAs, since drm1 drm2 cmt3 triple mutants show a lack of non-CpG methylation but elevated levels of siRNAs. Finally, we demonstrate that DRM activity is required for the initial establishment of RdDM in all sequence contexts including CpG, CpNpG, and asymmetric sites.}, author = {Cao, Xiaofeng and Aufsatz, Werner and Zilberman, Daniel and Mette, M.Florian and Huang, Michael S. and Matzke, Marjori and Jacobsen, Steven E.}, issn = {1879-0445}, journal = {Current Biology}, number = {24}, pages = {2212--2217}, publisher = {Elsevier}, title = {{Role of the DRM and CMT3 methyltransferases in RNA-directed DNA methylation}}, doi = {10.1016/j.cub.2003.11.052}, volume = {13}, year = {2003}, } @article{4169, abstract = {Background: During vertebrate gastrulation, cell polarization and migration are core components in the cellular rearrangements that lead to the formation of the three germ layers, ectoderm, mesoderm, and endoderm. Previous studies have implicated the Wnt/planar cell polarity (PCP) signaling pathway in controlling cell morphology and movement during gastrulation. However, cell polarization and directed cell migration are reduced but not completely abolished in the absence of Wnt/PCP signals; this observation indicates that other signaling pathways must be involved. Results: We show that Phosphoinositide 3-Kinases (PI3Ks) are required at the onset of zebrafish gastrulation in mesendodermal cells for process formation and cell polarization. Platelet Derived Growth Factor (PDGF) functions upstream of PI3K, while Protein Kinase B (PKB), a downstream effector of PI3K activity, localizes to the leading edge of migrating mesendodermal cells. In the absence of PI3K activity, PKB localization and cell polarization are strongly reduced in mesendodermal cells and are followed by slower but still highly coordinated and directed movements of these cells. Conclusions: We have identified a novel role of a signaling pathway comprised of PDGF, PI3K, and PKB in the control of morphogenetic cell movements during gastrulation. Furthermore, our findings provide insight into the relationship between cell polarization and directed cell migration at the onset of zebrafish gastrulation.}, author = {Montero, Juan and Kilian, Beate and Chan, Joanne and Bayliss, Peter and Heisenberg, Carl-Philipp J}, issn = {1879-0445}, journal = {Current Biology}, number = {15}, pages = {1279 -- 1289}, publisher = {Cell Press}, title = {{Phosphoinositide 3-kinase is required for process outgrowth and cell polarization of gastrulating mesendodermal cells}}, doi = {10.1016/S0960-9822(03)00505-0}, volume = {13}, year = {2003}, } @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}, }