The Experts below are selected from a list of 2526 Experts worldwide ranked by ideXlab platform
Claudia Köhler - One of the best experts on this subject based on the ideXlab platform.
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an imprinted gene underlies postzygotic reproductive isolation in arabidopsis thaliana
Developmental Cell, 2013Co-Authors: David Kradolfer, Philip Wolff, Alexey Siretskiy, Hua Jiang, Claudia KöhlerAbstract:Postzygotic reproductive isolation in response to interploidy hybridizations is a well-known phenomenon in plants that forms a major path for sympatric speciation. A main determinant for the failure of interploidy hybridizations is the endosperm, a nutritious tissue supporting embryo growth, similar to the functional role of the placenta in mammals. Although it has been suggested that deregulated imprinted genes underpin dosage sensitivity of the endosperm, the molecular basis for this phenomenon remained unknown. In a genetic screen for suppressors of triploid Seed Abortion, we have identified the paternally expressed imprinted gene ADMETOS (ADM). Here, we present evidence that increased dosage of ADM causes triploid Seed arrest. A large body of theoretical work predicted that deregulated imprinted genes establish the barrier to interploidy hybridization. Our study thus provides evidence strongly supporting this hypothesis and generates the molecular basis for our understanding of postzygotic hybridization barriers in plants.
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h3k27me3 profiling of the endosperm implies exclusion of polycomb group protein targeting by dna methylation
PLOS Genetics, 2010Co-Authors: Isabelle Weinhofer, Claudia Köhler, Lars Hennig, Elisabeth Hehenberger, Pawel RoszakAbstract:Polycomb group (PcG) proteins act as evolutionary conserved epigenetic mediators of cell identity because they repress transcriptional programs that are not required at particular developmental stages. Each tissue is likely to have a specific epigenetic profile, which acts as a blueprint for its developmental fate. A hallmark for Polycomb Repressive Complex 2 (PRC2) activity is trimethylated lysine 27 on histone H3 (H3K27me3). In plants, there are distinct PRC2 complexes for vegetative and reproductive development, and it was unknown so far whether these complexes have target gene specificity. The FERTILIZATION INDEPENDENT Seed (FIS) PRC2 complex is specifically expressed in the endosperm and is required for its development; loss of FIS function causes endosperm hyperproliferation and Seed Abortion. The endosperm nourishes the embryo, similar to the physiological function of the placenta in mammals. We established the endosperm H3K27me3 profile and identified specific target genes of the FIS complex with functional roles in endosperm cellularization and chromatin architecture, implicating that distinct PRC2 complexes have a subset of specific target genes. Importantly, our study revealed that selected transposable elements and protein coding genes are specifically targeted by the FIS PcG complex in the endosperm, whereas these elements and genes are densely marked by DNA methylation in vegetative tissues, suggesting that DNA methylation prevents targeting by PcG proteins in vegetative tissues.
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imprinting of the polycomb group gene medea serves as a ploidy sensor in arabidopsis
PLOS Genetics, 2009Co-Authors: Aleksandra Erilova, Lars Hennig, Lynette Brownfield, Vivien Exner, Marisa Rosa, David Twell, Ortrun Mittelsten Scheid, Claudia KöhlerAbstract:Balanced maternal and paternal genome contributions are a requirement for successful Seed development. Unbalanced contributions often cause Seed Abortion, a phenomenon that has been termed “triploid block.” Misregulation of imprinted regulatory genes has been proposed to be the underlying cause for abnormalities in growth and structure of the endosperm in Seeds with deviating parental contributions. We identified a mutant forming unreduced pollen that enabled us to investigate direct effects of unbalanced parental genome contributions on Seed development and to reveal the underlying molecular mechanism of dosage sensitivity. We provide evidence that parent-of-origin–specific expression of the Polycomb group (PcG) gene MEDEA is causally responsible for Seed developmental aberrations in Arabidopsis Seeds with increased paternal genome contributions. We propose that imprinted expression of PcG genes is an evolutionary conserved mechanism to balance parental genome contributions in embryo nourishing tissues.
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arabidopsis msi1 is a component of the mea fie polycomb group complex and required for Seed development
The EMBO Journal, 2003Co-Authors: Claudia Köhler, Ueli Grossniklaus, Jacqueline Gheyselinck, Lars Hennig, Romaric Bouveret, Wilhelm GruissemAbstract:Seed development in angiosperms initiates after double fertilization, leading to the formation of a diploid embryo and a triploid endosperm. The active repression of precocious initiation of certain aspects of Seed development in the absence of fertilization requires the Polycomb group proteins MEDEA (MEA), FERTILIZATION-INDEPENDENT ENDOSPERM (FIE) and FERTILIZATION-INDEPENDENT Seed2. Here we show that the Arabidopsis WD-40 domain protein MSI1 is present together with MEA and FIE in a 600 kDa complex and interacts directly with FIE. Mutant plants heterozygous for msi1 show a Seed Abortion ratio of 50% with Seeds aborting when the mutant allele is maternally inherited, irrespective of a paternal wild-type or mutant MSI1 allele. Further more, msi1 mutant gametophytes initiate endosperm development in the absence of fertilization at a high penetrance. After pollination, only the egg cell becomes fertilized, the central cell starts dividing prior to fertilization, resulting in the formation of Seeds containing embryos surrounded by diploid endosperm. Our results establish that MSI1 has an essential function in the correct initiation and progression of Seed development.
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the polycomb group protein medea regulates Seed development by controlling expression of the mads box gene pheres1
Genes & Development, 2003Co-Authors: Claudia Köhler, Lars Hennig, Wilhelm Gruissem, Charles Spillane, Stephane Pien, Ueli GrossniklausAbstract:The Polycomb-group (PcG) proteins MEDEA, FERTILIZATION INDEPENDENT ENDOSPERM, and FERTILIZATION INDEPENDENT Seed2 regulate Seed development in Arabidopsis by controlling embryo and endosperm proliferation. All three of these FIS-class proteins are likely subunits of a multiprotein PcG complex, which epigenetically regulates downstream target genes that were previously unknown. Here we show that the MADS-box gene PHERES1 (PHE1) is commonly deregulated in the fis-class mutants. PHE1 belongs to the evolutionarily ancient type I class of MADS-box proteins that have not yet been assigned any function in plants. Both MEDEA and FIE directly associate with the promoter region of PHE1, suggesting that PHE1 expression is epigenetically regulated by PcG proteins. PHE1 is expressed transiently after fertilization in both the embryo and the endosperm; however, it remains up-regulated in the fis mutants, consistent with the proposed function of the FIS genes as transcriptional repressors. Reduced expression levels of PHE1 in medea mutant Seeds can suppress medea Seed Abortion, indicating a key role of PHE1 repression in Seed development. PHE1 expression in a hypomethylated medea mutant background resembles the wild-type expression pattern and is associated with rescue of the medea Seed-Abortion phenotype. In summary, our results demonstrate that Seed Abortion in the medea mutant is largely mediated by deregulated expression of the type I MADS-box gene PHE1.
Richard D Vierstra - One of the best experts on this subject based on the ideXlab platform.
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the vacuolar protein sorting 38 subunit of the arabidopsis phosphatidylinositol 3 kinase complex plays critical roles in autophagy endosome sorting and gravitropism
Frontiers in Plant Science, 2018Co-Authors: Weiming Hu, Richard D VierstraAbstract:The family of phosphatidylinositols (PtdIns) plays essential roles in membrane identity and intracellular trafficking events. In animals and yeast, PtdIn-3-phosphate, which is particularly important for endosomal sorting, lysosomal/vacuolar transport and autophagy, is assembled by two conserved kinase complexes comprised of the catalytic VACUOLAR PROTEIN SORTING (VPS)-34 subunit, along with VPS15, AUTOPHAGY-RELATED (ATG)-6, and either ATG14 (complex I) or VPS38 (complex II). Here, we describe the Arabidopsis ortholog of VPS38 and show by interaction assays that it assembles into a tetrameric PtdIn-3 kinase complex II. Plants missing VPS38 are viable but have dampened pollen germination and heightened Seed Abortion, and display a dwarf rosette phenotype, with defects in leaf and vascular development and sucrose sensing. vps38 Seeds accumulate irregular protein storage vesicles and suppress processing of storage proteins into their mature forms. Consistent with a role for PtdIn-3-phosphate in autophagy, vps38 mutants are hypersensitive to nitrogen and fixed-carbon starvation and show reduced autophagic transport of cargo into vacuoles. vps38 Seedlings also have dampened root gravitropism, which is underpinned by aberrant vectoral auxin transport likely caused by defects in plasma membrane/endosome cycling of the PIN-FORMED family of auxin transporters necessary for asymmetric cell elongation. Collectively, this study places VPS38 and its class-III PtdIn-3 kinase complex at the nexus of numerous endosomal trafficking events important to plant growth and development.
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Image_1_The Vacuolar Protein Sorting-38 Subunit of the Arabidopsis Phosphatidylinositol-3-Kinase Complex Plays Critical Roles in Autophagy, Endosome Sorting, and Gravitropism.pdf
2018Co-Authors: Fen Liu, Richard D VierstraAbstract:The family of phosphatidylinositols (PtdIns) plays essential roles in membrane identity and intracellular trafficking events. In animals and yeast, PtdIn-3-phosphate, which is particularly important for endosomal sorting, lysosomal/vacuolar transport and autophagy, is assembled by two conserved kinase complexes comprised of the catalytic VACUOLAR PROTEIN SORTING (VPS)-34 subunit, along with VPS15, AUTOPHAGY-RELATED (ATG)-6, and either ATG14 (complex I) or VPS38 (complex II). Here, we describe the Arabidopsis ortholog of VPS38 and show by interaction assays that it assembles into a tetrameric PtdIn-3 kinase complex II. Plants missing VPS38 are viable but have dampened pollen germination and heightened Seed Abortion, and display a dwarf rosette phenotype, with defects in leaf and vascular development and sucrose sensing. vps38 Seeds accumulate irregular protein storage vesicles and suppress processing of storage proteins into their mature forms. Consistent with a role for PtdIn-3-phosphate in autophagy, vps38 mutants are hypersensitive to nitrogen and fixed-carbon starvation and show reduced autophagic transport of cargo into vacuoles. vps38 Seedlings also have dampened root gravitropism, which is underpinned by aberrant vectoral auxin transport likely caused by defects in plasma membrane/endosome cycling of the PIN-FORMED family of auxin transporters necessary for asymmetric cell elongation. Collectively, this study places VPS38 and its class-III PtdIn-3 kinase complex at the nexus of numerous endosomal trafficking events important to plant growth and development.
Lars Hennig - One of the best experts on this subject based on the ideXlab platform.
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h3k27me3 profiling of the endosperm implies exclusion of polycomb group protein targeting by dna methylation
PLOS Genetics, 2010Co-Authors: Isabelle Weinhofer, Claudia Köhler, Lars Hennig, Elisabeth Hehenberger, Pawel RoszakAbstract:Polycomb group (PcG) proteins act as evolutionary conserved epigenetic mediators of cell identity because they repress transcriptional programs that are not required at particular developmental stages. Each tissue is likely to have a specific epigenetic profile, which acts as a blueprint for its developmental fate. A hallmark for Polycomb Repressive Complex 2 (PRC2) activity is trimethylated lysine 27 on histone H3 (H3K27me3). In plants, there are distinct PRC2 complexes for vegetative and reproductive development, and it was unknown so far whether these complexes have target gene specificity. The FERTILIZATION INDEPENDENT Seed (FIS) PRC2 complex is specifically expressed in the endosperm and is required for its development; loss of FIS function causes endosperm hyperproliferation and Seed Abortion. The endosperm nourishes the embryo, similar to the physiological function of the placenta in mammals. We established the endosperm H3K27me3 profile and identified specific target genes of the FIS complex with functional roles in endosperm cellularization and chromatin architecture, implicating that distinct PRC2 complexes have a subset of specific target genes. Importantly, our study revealed that selected transposable elements and protein coding genes are specifically targeted by the FIS PcG complex in the endosperm, whereas these elements and genes are densely marked by DNA methylation in vegetative tissues, suggesting that DNA methylation prevents targeting by PcG proteins in vegetative tissues.
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imprinting of the polycomb group gene medea serves as a ploidy sensor in arabidopsis
PLOS Genetics, 2009Co-Authors: Aleksandra Erilova, Lars Hennig, Lynette Brownfield, Vivien Exner, Marisa Rosa, David Twell, Ortrun Mittelsten Scheid, Claudia KöhlerAbstract:Balanced maternal and paternal genome contributions are a requirement for successful Seed development. Unbalanced contributions often cause Seed Abortion, a phenomenon that has been termed “triploid block.” Misregulation of imprinted regulatory genes has been proposed to be the underlying cause for abnormalities in growth and structure of the endosperm in Seeds with deviating parental contributions. We identified a mutant forming unreduced pollen that enabled us to investigate direct effects of unbalanced parental genome contributions on Seed development and to reveal the underlying molecular mechanism of dosage sensitivity. We provide evidence that parent-of-origin–specific expression of the Polycomb group (PcG) gene MEDEA is causally responsible for Seed developmental aberrations in Arabidopsis Seeds with increased paternal genome contributions. We propose that imprinted expression of PcG genes is an evolutionary conserved mechanism to balance parental genome contributions in embryo nourishing tissues.
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arabidopsis msi1 is a component of the mea fie polycomb group complex and required for Seed development
The EMBO Journal, 2003Co-Authors: Claudia Köhler, Ueli Grossniklaus, Jacqueline Gheyselinck, Lars Hennig, Romaric Bouveret, Wilhelm GruissemAbstract:Seed development in angiosperms initiates after double fertilization, leading to the formation of a diploid embryo and a triploid endosperm. The active repression of precocious initiation of certain aspects of Seed development in the absence of fertilization requires the Polycomb group proteins MEDEA (MEA), FERTILIZATION-INDEPENDENT ENDOSPERM (FIE) and FERTILIZATION-INDEPENDENT Seed2. Here we show that the Arabidopsis WD-40 domain protein MSI1 is present together with MEA and FIE in a 600 kDa complex and interacts directly with FIE. Mutant plants heterozygous for msi1 show a Seed Abortion ratio of 50% with Seeds aborting when the mutant allele is maternally inherited, irrespective of a paternal wild-type or mutant MSI1 allele. Further more, msi1 mutant gametophytes initiate endosperm development in the absence of fertilization at a high penetrance. After pollination, only the egg cell becomes fertilized, the central cell starts dividing prior to fertilization, resulting in the formation of Seeds containing embryos surrounded by diploid endosperm. Our results establish that MSI1 has an essential function in the correct initiation and progression of Seed development.
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the polycomb group protein medea regulates Seed development by controlling expression of the mads box gene pheres1
Genes & Development, 2003Co-Authors: Claudia Köhler, Lars Hennig, Wilhelm Gruissem, Charles Spillane, Stephane Pien, Ueli GrossniklausAbstract:The Polycomb-group (PcG) proteins MEDEA, FERTILIZATION INDEPENDENT ENDOSPERM, and FERTILIZATION INDEPENDENT Seed2 regulate Seed development in Arabidopsis by controlling embryo and endosperm proliferation. All three of these FIS-class proteins are likely subunits of a multiprotein PcG complex, which epigenetically regulates downstream target genes that were previously unknown. Here we show that the MADS-box gene PHERES1 (PHE1) is commonly deregulated in the fis-class mutants. PHE1 belongs to the evolutionarily ancient type I class of MADS-box proteins that have not yet been assigned any function in plants. Both MEDEA and FIE directly associate with the promoter region of PHE1, suggesting that PHE1 expression is epigenetically regulated by PcG proteins. PHE1 is expressed transiently after fertilization in both the embryo and the endosperm; however, it remains up-regulated in the fis mutants, consistent with the proposed function of the FIS genes as transcriptional repressors. Reduced expression levels of PHE1 in medea mutant Seeds can suppress medea Seed Abortion, indicating a key role of PHE1 repression in Seed development. PHE1 expression in a hypomethylated medea mutant background resembles the wild-type expression pattern and is associated with rescue of the medea Seed-Abortion phenotype. In summary, our results demonstrate that Seed Abortion in the medea mutant is largely mediated by deregulated expression of the type I MADS-box gene PHE1.
Weiming Hu - One of the best experts on this subject based on the ideXlab platform.
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the vacuolar protein sorting 38 subunit of the arabidopsis phosphatidylinositol 3 kinase complex plays critical roles in autophagy endosome sorting and gravitropism
Frontiers in Plant Science, 2018Co-Authors: Weiming Hu, Richard D VierstraAbstract:The family of phosphatidylinositols (PtdIns) plays essential roles in membrane identity and intracellular trafficking events. In animals and yeast, PtdIn-3-phosphate, which is particularly important for endosomal sorting, lysosomal/vacuolar transport and autophagy, is assembled by two conserved kinase complexes comprised of the catalytic VACUOLAR PROTEIN SORTING (VPS)-34 subunit, along with VPS15, AUTOPHAGY-RELATED (ATG)-6, and either ATG14 (complex I) or VPS38 (complex II). Here, we describe the Arabidopsis ortholog of VPS38 and show by interaction assays that it assembles into a tetrameric PtdIn-3 kinase complex II. Plants missing VPS38 are viable but have dampened pollen germination and heightened Seed Abortion, and display a dwarf rosette phenotype, with defects in leaf and vascular development and sucrose sensing. vps38 Seeds accumulate irregular protein storage vesicles and suppress processing of storage proteins into their mature forms. Consistent with a role for PtdIn-3-phosphate in autophagy, vps38 mutants are hypersensitive to nitrogen and fixed-carbon starvation and show reduced autophagic transport of cargo into vacuoles. vps38 Seedlings also have dampened root gravitropism, which is underpinned by aberrant vectoral auxin transport likely caused by defects in plasma membrane/endosome cycling of the PIN-FORMED family of auxin transporters necessary for asymmetric cell elongation. Collectively, this study places VPS38 and its class-III PtdIn-3 kinase complex at the nexus of numerous endosomal trafficking events important to plant growth and development.
Meng-xiang Sun - One of the best experts on this subject based on the ideXlab platform.
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A bipartite molecular module controls cell death activation in the Basal cell lineage of plant embryos.
PLoS Biology, 2013Co-Authors: Peng Zhao, Wei Wang, Li-yao Zhang, Xiongbo Peng, Xue-mei Zhou, Li-bo Yang, Peter V. Bozhkov, Meng-xiang SunAbstract:Plant zygote divides asymmetrically into an apical cell that develops into the embryo proper and a basal cell that generates the suspensor, a vital organ functioning as a conduit of nutrients and growth factors to the embryo proper. After the suspensor has fulfilled its function, it is removed by programmed cell death (PCD) at the late stages of embryogenesis. The molecular trigger of this PCD is unknown. Here we use tobacco (Nicotiana tabacum) embryogenesis as a model system to demonstrate that the mechanism triggering suspensor PCD is based on the antagonistic action of two proteins: a protease inhibitor, cystatin NtCYS, and its target, cathepsin H-like protease NtCP14. NtCYS is expressed in the basal cell of the proembryo, where encoded cystatin binds to and inhibits NtCP14, thereby preventing precocious onset of PCD. The anti-cell death effect of NtCYS is transcriptionally regulated and is repressed at the 32-celled embryo stage, leading to increased NtCP14 activity and initiation of PCD. Silencing of NtCYS or overexpression of NtCP14 induces precocious cell death in the basal cell lineage causing embryonic arrest and Seed Abortion. Conversely, overexpression of NtCYS or silencing of NtCP14 leads to profound delay of suspensor PCD. Our results demonstrate that NtCYS-mediated inhibition of NtCP14 protease acts as a bipartite molecular module to control initiation of PCD in the basal cell lineage of plant embryos.
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A Bipartite Molecular Module Controls Cell Death Activation in the Basal Cell Lineage of Plant Embryos
2013Co-Authors: Peter V. Bozhkov, Meng-xiang SunAbstract:Plant zygote divides asymmetrically into an apical cell that develops into the embryo proper and a basal cell that generates the suspensor, a vital organ functioning as a conduit of nutrients and growth factors to the embryo proper. After the suspensor has fulfilled its function, it is removed by programmed cell death (PCD) at the late stages of embryogenesis. The molecular trigger of this PCD is unknown. Here we use tobacco (Nicotiana tabacum) embryogenesis as a model system to demonstrate that the mechanism triggering suspensor PCD is based on the antagonistic action of two proteins: a protease inhibitor, cystatin NtCYS, and its target, cathepsin H-like protease NtCP14. NtCYS is expressed in the basal cell of the proembryo, where encoded cystatin binds to and inhibits NtCP14, thereby preventing precocious onset of PCD. The anti-cell death effect of NtCYS is transcriptionally regulated and is repressed at the 32-celled embryo stage, leading to increased NtCP14 activity and initiation of PCD. Silencing of NtCYS or overexpression of NtCP14 induces precocious cell death in the basal cell lineage causing embryonic arrest and Seed Abortion. Conversely, overexpression of NtCYS or silencing of NtCP14 leads to profound delay of suspensor PCD. Our results demonstrate that NtCYS-mediated inhibition of NtCP14 protease acts as a bipartite molecular module to contro