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  • 1. Baud, Sébastien
    et al.
    Bellec, Yannick
    Miquel, Martine
    Bellini, Catherine
    Caboche, Michel
    Lepiniec, Loïc
    Faure, Jean-Denis
    Rochat, Christine
    gurke and pasticcino3 mutants affected in embryo development are impaired in acetyl-CoA carboxylase.2004Ingår i: EMBO Reports, ISSN 1469-221X, E-ISSN 1469-3178, Vol. 5, nr 5Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Normal embryo development is required for correct seedling formation. The Arabidopsis gurke and pasticcino3 mutants were isolated from different developmental screens and the corresponding embryos exhibit severe defects in their apical region, affecting bilateral symmetry. We have recently identified lethal acc1 mutants affected in acetyl-CoA carboxylase 1 (ACCase 1) that display a similar embryo phenotype. A series of crosses showed that gk and pas3 are allelic to acc1 mutants, and direct sequencing of the ACC1 gene revealed point mutations in these new alleles. The isolation of leaky acc1 alleles demonstrated that ACCase 1 is essential for correct plant development and that mutations in ACCase affect cellular division in plants, as is the case in yeast. Interestingly, significant metabolic complementation of the mutant phenotype was obtained by exogenous supply of malonate, suggesting that the lack of cytosolic malonyl-CoA is likely to be the initial factor leading to abnormal development in the acc1 mutants.

  • 2. Cruz Alsina, Fernando
    et al.
    Javier Hita, Francisco
    Aldana Fontanet, Paula
    Irala, Dolores
    Hedman, Håkan
    Umeå universitet, Medicinska fakulteten, Institutionen för strålningsvetenskaper, Onkologi.
    Ledda, Fernanda
    Paratcha, Gustavo
    Lrig1 is a cell-intrinsic modulator of hippocampal dendrite complexity and BDNF signaling2016Ingår i: EMBO Reports, ISSN 1469-221X, E-ISSN 1469-3178, Vol. 17, nr 4, s. 601-616Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Even though many extracellular factors have been identified as promoters of general dendritic growth and branching, little is known about the cell-intrinsic modulators that allow neurons to sculpt distinctive patterns of dendrite arborization. Here, we identify Lrig1, a nervous system-enriched LRR protein, as a key physiological regulator of dendrite complexity of hippocampal pyramidal neurons. Lrig1-deficient mice display morphological changes in proximal dendrite arborization and defects in social interaction. Specifically, knockdown of Lrig1 enhances both primary dendrite formation and proximal dendritic branching of hippocampal neurons, two phenotypes that resemble the effect of BDNF on these neurons. In addition, we show that Lrig1 physically interacts with TrkB and attenuates BDNF signaling. Gain and loss of function assays indicate that Lrig1 restricts BDNF-induced dendrite morphology. Together, our findings reveal a novel and essential role of Lrig1 in regulating morphogenic events that shape the hippocampal circuits and establish that the assembly of TrkB with Lrig1 represents a key mechanism for understanding how specific neuronal populations expand the repertoire of responses to BDNF during brain development.

  • 3.
    Dorafshan, Eshagh
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för molekylärbiologi (Medicinska fakulteten).
    Kahn, Tatyana G.
    Umeå universitet, Medicinska fakulteten, Institutionen för molekylärbiologi (Medicinska fakulteten).
    Glotov, Alexander
    Umeå universitet, Medicinska fakulteten, Institutionen för molekylärbiologi (Medicinska fakulteten).
    Savitsky, Mikhail
    Umeå universitet, Medicinska fakulteten, Institutionen för molekylärbiologi (Medicinska fakulteten).
    Walther, Matthias
    Reuter, Gunter
    Schwartz, Yuri B.
    Umeå universitet, Medicinska fakulteten, Institutionen för molekylärbiologi (Medicinska fakulteten).
    Ash1 counteracts Polycomb repression independent of histone H3 lysine 36 methylation2019Ingår i: EMBO Reports, ISSN 1469-221X, E-ISSN 1469-3178, Vol. 20, nr 4, artikel-id e46762Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Polycomb repression is critical for metazoan development. Equally important but less studied is the Trithorax system, which safeguards Polycomb target genes from the repression in cells where they have to remain active. It was proposed that the Trithorax system acts via methylation of histone H3 at lysine 4 and lysine 36 (H3K36), thereby inhibiting histone methyltransferase activity of the Polycomb complexes. Here we test this hypothesis by asking whether the Trithorax group protein Ash1 requires H3K36 methylation to counteract Polycomb repression. We show that Ash1 is the only Drosophila H3K36-specific methyltransferase necessary to prevent excessive Polycomb repression of homeotic genes. Unexpectedly, our experiments reveal no correlation between the extent of H3K36 methylation and the resistance to Polycomb repression. Furthermore, we find that complete substitution of the zygotic histone H3 with a variant in which lysine 36 is replaced by arginine does not cause excessive repression of homeotic genes. Our results suggest that the model, where the Trithorax group proteins methylate histone H3 to inhibit the histone methyltransferase activity of the Polycomb complexes, needs revision.

  • 4.
    Fällman, Erik
    et al.
    Umeå universitet, Teknisk-naturvetenskapliga fakulteten, Institutionen för fysik.
    Schedin, Staffan
    Umeå universitet, Teknisk-naturvetenskapliga fakulteten, Institutionen för tillämpad fysik och elektronik.
    Jass, Jana
    Department of Microbiology and Immunology, The Lawson Health Research Institute, University of Western Ontario, London, Ontario, Canada.
    Uhlin, Bernt Eric
    Umeå universitet, Medicinska fakulteten, Institutionen för molekylärbiologi (Medicinska fakulteten).
    Axner, Ove
    Umeå universitet, Teknisk-naturvetenskapliga fakulteten, Institutionen för fysik.
    The unfolding of the P pili quaternary structure by stretching is reversible, not plastic2005Ingår i: EMBO Reports, ISSN 1469-221X, E-ISSN 1469-3178, Vol. 6, nr 1, s. 52-56Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    P pili are protein filaments expressed by uropathogenic Escherichia coli that mediate binding to glycolipids on epithelial cell surfaces, which is a prerequisite for bacterial infection. When a bacterium, attached to a cell surface, is exposed to external forces, the pili, which are composed of ∼103PapA protein subunits arranged in a helical conformation, can elongate by unfolding to a linear conformation. This property is considered important for the ability of a bacterium to withstand shear forces caused by urine flow. It has hitherto been assumed that this elongation is plastic, thus constituting a permanent conformational deformation. We demonstrate, using optical tweezers, that this is not the case; the unfolding of the helical structure to a linear conformation is fully reversible. It is surmised that this reversibility helps the bacteria regain close contact to the host cells after exposure to significant shear forces, which is believed to facilitate their colonization.

  • 5.
    Lorén, Christina
    et al.
    Umeå universitet, Teknisk-naturvetenskapliga fakulteten, Umeå centrum för molekylär patogenes (UCMP).
    Englund, Camilla
    Umeå universitet, Teknisk-naturvetenskapliga fakulteten, Umeå centrum för molekylär patogenes (UCMP).
    Grabbe, Caroline
    Umeå universitet, Teknisk-naturvetenskapliga fakulteten, Umeå centrum för molekylär patogenes (UCMP).
    Hallberg, Bengt
    Umeå universitet, Medicinska fakulteten, Institutionen för medicinsk biovetenskap, Patologi.
    Hunter, Tony
    Palmer, Ruth H
    Umeå universitet, Teknisk-naturvetenskapliga fakulteten, Umeå centrum för molekylär patogenes (UCMP).
    A crucial role for the Anaplastic lymphoma kinase receptor tyrosine kinase in gut development in Drosophila melanogaster2003Ingår i: EMBO Reports, ISSN 1469-221X, E-ISSN 1469-3178, Vol. 4, nr 8, s. 781-786Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The Drosophila melanogaster gene Anaplastic lymphoma kinase (Alk) is homologous to mammalian Alk, which encodes a member of the Alk/Ltk family of receptor tyrosine kinases (RTKs). In humans, the t(2;5) translocation, which involves the ALK locus, produces an active form of ALK, which is the causative agent in non-Hodgkin's lymphoma. The physiological function of the Alk RTK, however, is unknown. In this paper, we describe loss-of-function mutants in the Drosophila Alk gene that cause a complete failure of the development of the gut. We propose that the main function of Drosophila Alk during early embryogenesis is in visceral mesoderm development.

  • 6.
    Sobhy, Haitham
    Umeå universitet, Teknisk-naturvetenskapliga fakulteten, Institutionen för molekylärbiologi (Teknisk-naturvetenskaplig fakultet).
    Social influence and peer review - impact factor and citation2016Ingår i: EMBO Reports, ISSN 1469-221X, E-ISSN 1469-3178, Vol. 17, nr 4, s. 473-473Artikel i tidskrift (Refereegranskat)
  • 7. Styer, Katie L
    et al.
    Hopkins, Gregory W
    Bartra, Sara Schesser
    3Department of Microbiology & Immunology, University of Miami School of Medicine, Miami, Florida, USA.
    Plano, Gregory V
    Frothingham, Richard
    Aballay, Alejandro
    Yersinia pestis kills Caenorhabditis elegans by a biofilm-independent process that involves novel virulence factors.2005Ingår i: EMBO Reports, ISSN 1469-221X, E-ISSN 1469-3178, Vol. 6, nr 10, s. 992-997Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    It is known that Yersinia pestis kills Caenorhabditis elegans by a biofilm-dependent mechanism that is similar to the mechanism used by the pathogen to block food intake in the flea vector. Using Y. pestis KIM 5, which lacks the genes that are required for biofilm formation, we show that Y. pestis can kill C. elegans by a biofilm-independent mechanism that correlates with the accumulation of the pathogen in the intestine. We used this novel Y. pestis-C. elegans pathogenesis system to show that previously known and unknown virulence-related genes are required for full virulence in C. elegans. Six Y. pestis mutants with insertions in genes that are not related to virulence before were isolated using C. elegans. One of the six mutants carried an insertion in a novel virulence gene and showed significantly reduced virulence in a mouse model of Y. pestis pathogenesis. Our results indicate that the Y. pestis-C. elegans pathogenesis system that is described here can be used to identify and study previously uncharacterized Y. pestis gene products required for virulence in mammalian systems.

  • 8. Søreng, Kristiane
    et al.
    Munson, Michael J.
    Lamb, Christopher A.
    Bjørndal, Gunnveig T.
    Pankiv, Serhiy
    Carlsson, Sven R.
    Umeå universitet, Medicinska fakulteten, Institutionen för medicinsk kemi och biofysik.
    Tooze, Sharon A.
    Simonsen, Anne
    SNX18 regulates ATG9A trafficking from recycling endosomes by recruiting Dynamin-22018Ingår i: EMBO Reports, ISSN 1469-221X, E-ISSN 1469-3178, Vol. 19, nr 4, artikel-id e44837Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Trafficking of mammalian ATG9A between the Golgi apparatus, endosomes and peripheral ATG9A compartments is important for autophagosome biogenesis. Here, we show that the membrane remodelling protein SNX18, previously identified as a positive regulator of autophagy, regulates ATG9A trafficking from recycling endosomes. ATG9A is recruited to SNX18-induced tubules generated from recycling endosomes and accumulates in juxtanuclear recycling endosomes in cells lacking SNX18. Binding of SNX18 to Dynamin-2 is important for ATG9A trafficking from recycling endosomes and for formation of ATG16L1- and WIPI2-positive autophagosome precursor membranes. We propose a model where upon autophagy induction, SNX18 recruits Dynamin-2 to induce budding of ATG9A and ATG16L1 containing membranes from recycling endosomes that traffic to sites of autophagosome formation.

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  • 9. von Hofsten, Jonas
    et al.
    Elworthy, Stone
    Gilchrist, Michael J
    Smith, James C
    Wardle, Fiona C
    Ingham, Philip W
    Prdm1- and Sox6-mediated transcriptional repression specifies muscle fibre type in the zebrafish embryo2008Ingår i: EMBO Reports, ISSN 1469-221X, E-ISSN 1469-3178, Vol. 9, nr 7, s. 683-689Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The zebrafish u-boot (ubo) gene encodes the transcription factor Prdm1, which is essential for the specification of the primary slow-twitch muscle fibres that derive from adaxial cells. Here, we show that Prdm1 functions by acting as a transcriptional repressor and that slow-twitch-specific muscle gene expression is activated by Prdm1-mediated repression of the transcriptional repressor Sox6. Genes encoding fast-specific isoforms of sarcomeric proteins are ectopically expressed in the adaxial cells of ubo(tp39) mutant embryos. By using chromatin immunoprecipitation, we show that these are direct targets of Prdm1. Thus, Prdm1 promotes slow-twitch fibre differentiation by acting as a global repressor of fast-fibre-specific genes, as well as by abrogating the repression of slow-fibre-specific genes.

  • 10.
    Yang, Hairu
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för molekylärbiologi (Medicinska fakulteten).
    Kronhamn, Jesper
    Umeå universitet, Medicinska fakulteten, Institutionen för molekylärbiologi (Medicinska fakulteten).
    Ekstrom, Jens-Ola
    Umeå universitet, Medicinska fakulteten, Institutionen för molekylärbiologi (Medicinska fakulteten).
    Korkut, Gul Gizem
    Umeå universitet, Medicinska fakulteten, Institutionen för molekylärbiologi (Medicinska fakulteten).
    Hultmark, Dan
    Umeå universitet, Medicinska fakulteten, Institutionen för molekylärbiologi (Medicinska fakulteten).
    JAK/STAT signaling in Drosophila muscles controls the cellular immune response against parasitoid infection2015Ingår i: EMBO Reports, ISSN 1469-221X, E-ISSN 1469-3178, Vol. 16, nr 12, s. 1664-1672Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The role of JAK/STAT signaling in the cellular immune response of Drosophila is not well understood. Here, we show that parasitoid wasp infection activates JAK/STAT signaling in somatic muscles of the Drosophila larva, triggered by secretion of the cytokines Upd2 and Upd3 from circulating hemocytes. Deletion of upd2 or upd3, but not the related os (upd1) gene, reduced the cellular immune response, and suppression of the JAK/STAT pathway in muscle cells reduced the encapsulation of wasp eggs and the number of circulating lamellocyte effector cells. These results suggest that JAK/STAT signaling in muscles participates in a systemic immune defense against wasp infection.

  • 11.
    Zheng, Wenjing
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för medicinsk kemi och biofysik.
    Gorre, Nagaraju
    Umeå universitet, Medicinska fakulteten, Institutionen för medicinsk kemi och biofysik.
    Shen, Yue
    Umeå universitet, Medicinska fakulteten, Institutionen för medicinsk kemi och biofysik.
    Noda, Tetsuo
    Ogawa, Wataru
    Lundin, Eva
    Umeå universitet, Medicinska fakulteten, Institutionen för medicinsk biovetenskap, Patologi.
    Liu, Kui
    Umeå universitet, Medicinska fakulteten, Institutionen för medicinsk kemi och biofysik.
    Maternal phosphatidylinositol 3-kinase signalling is crucial for embryonic genome activation and preimplantation embryogenesis2010Ingår i: EMBO Reports, ISSN 1469-221X, E-ISSN 1469-3178, Vol. 11, nr 11, s. 890-895Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Maternal effect factors derived from oocytes are important for sustaining early embryonic development before the major wave of embryonic genome activation (EGA). In this study, we report a two-cell-stage arrest of embryos lacking maternal 3-phosphoinositide-dependent protein kinase 1 as a result of suppressed EGA. Concurrent deletion of maternal Pten completely rescued the suppressed EGA and embryonic progression through restored AKT signalling, which fully restored the fertility of double-mutant females. Our study identifies maternal phosphatidylinositol 3-kinase signalling as a new maternal effect factor that regulates EGA and preimplantation embryogenesis in mice.

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