- Seminars - maillist.psb.ugent.be

upcoming seminar February
by Nathalie Vanden Hautte 27 Jan '11

27 Jan '11

Dear All Enclosed you can find our upcoming seminar for February. Kind regards Nathalie ____________________________________________ Nathalie Vanden Hautte Administrative Assistant VIB, Department of Plant Systems Biology Ghent University Technologiepark 927 9052 Gent Belgium Phone: +32/9/33.13.800 Fax: +32/33.13.809 Http://www.psb.ugent.be nahau(a)psb.vib-ugent.be

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PSB event reminder
by contact＠psb.vib-ugent.be 20 Jan '11

20 Jan '11

Calendar Name: seminars Scheduled for: Thursday, January 20 2011, 11:00 - 12:30 Event text: Dr Wim Soppe Dept. of Plant Breeding and Genetics Max Planck Institute for Plant Breeding Research Cologne GERMANY Details: "Waking up in time, seed dormancy explained at the molecular level" ABSTRACT Viable plant seeds are not always able to germinate and can cycle between a dormant and a non-dormant state. Dormancy prevents germination during unfavourable seasons, an ability that has been lost in most of our crop species. In the model plant Arabidopsis, dormancy is induced during the maturation of seeds in the silique and released by imbibition of seeds at low temperatures (stratification) or dry storage (after-ripening). Seed dormancy is determined by the balance between the plant hormones abscisic acid and gibberellins. However, our knowledge about the molecular identity of dormancy and its control by environmental factors is limited. To reveal the molecular mechanisms that determine the induction and release of seed dormancy, my research group has analysed and cloned Arabidopsis mutants with reduced dormancy levels. The underlying genes could be divided in two groups. The first group contains ubiquitously expressed genes with a general role in plant development. Transcription factors, associated with elongating RNA polymerase II, are overrepresented in this group. Most of these genes are upregulated towards the end of seed maturation. Interestingly, this upregulation is correlated with a strong reduction in nuclear size during seed maturation. This suggests that RNA polymerase associated factors are required to facilitate gene expression in nuclei with reduced volume. An example of a gene belonging to this group is HUB1, which encodes a C3HC4 RING finger protein that is required for monoubiquitination of histone H2B. We observed altered expression levels for several dormancy genes in the hub1 mutant towards the end of seed maturation. The second group consists of dormancy genes with a seed-specific expression. The gene DELAY OF GERMINATION 1 (DOG1), which is expressed during seed maturation and encodes a protein with unknown function, belongs to this group. DOG1 is essential for seed dormancy because the dog1 mutant is completely non-dormant. DOG1 expression is upregulated by reduced temperatures during seed maturation. Higher levels of DOG1 protein in ripe seeds require an increasing after-ripening time to release seed dormancy. DOG1 is alternatively spliced and we have shown that DOG1 function requires binding between its different protein isoforms. In this seminar, I will present our present understanding of the molecular mechanism of seed dormancy in Arabidopsis and focus on the roles of RNA polymerase II associated factors and DOG1.

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PSB event reminder
by contact＠psb.vib-ugent.be 18 Jan '11

18 Jan '11

Calendar Name: seminars Scheduled for: Thursday, January 20 2011, 11:00 - 12:30 Event text: Dr Wim Soppe Dept. of Plant Breeding and Genetics Max Planck Institute for Plant Breeding Research Cologne GERMANY Details: "Waking up in time, seed dormancy explained at the molecular level" ABSTRACT Viable plant seeds are not always able to germinate and can cycle between a dormant and a non-dormant state. Dormancy prevents germination during unfavourable seasons, an ability that has been lost in most of our crop species. In the model plant Arabidopsis, dormancy is induced during the maturation of seeds in the silique and released by imbibition of seeds at low temperatures (stratification) or dry storage (after-ripening). Seed dormancy is determined by the balance between the plant hormones abscisic acid and gibberellins. However, our knowledge about the molecular identity of dormancy and its control by environmental factors is limited. To reveal the molecular mechanisms that determine the induction and release of seed dormancy, my research group has analysed and cloned Arabidopsis mutants with reduced dormancy levels. The underlying genes could be divided in two groups. The first group contains ubiquitously expressed genes with a general role in plant development. Transcription factors, associated with elongating RNA polymerase II, are overrepresented in this group. Most of these genes are upregulated towards the end of seed maturation. Interestingly, this upregulation is correlated with a strong reduction in nuclear size during seed maturation. This suggests that RNA polymerase associated factors are required to facilitate gene expression in nuclei with reduced volume. An example of a gene belonging to this group is HUB1, which encodes a C3HC4 RING finger protein that is required for monoubiquitination of histone H2B. We observed altered expression levels for several dormancy genes in the hub1 mutant towards the end of seed maturation. The second group consists of dormancy genes with a seed-specific expression. The gene DELAY OF GERMINATION 1 (DOG1), which is expressed during seed maturation and encodes a protein with unknown function, belongs to this group. DOG1 is essential for seed dormancy because the dog1 mutant is completely non-dormant. DOG1 expression is upregulated by reduced temperatures during seed maturation. Higher levels of DOG1 protein in ripe seeds require an increasing after-ripening time to release seed dormancy. DOG1 is alternatively spliced and we have shown that DOG1 function requires binding between its different protein isoforms. In this seminar, I will present our present understanding of the molecular mechanism of seed dormancy in Arabidopsis and focus on the roles of RNA polymerase II associated factors and DOG1.

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BARN Symposium: Growth and Development of Roots - Louvain-la-Neuve 27/01/11
by Christine Tire 12 Jan '11

12 Jan '11

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PSB event reminder
by contact＠psb.vib-ugent.be 06 Jan '11

06 Jan '11

Calendar Name: seminars Scheduled for: Thursday, January 6 2011, 11:00 - 12:30 Event text: Dr Arp Schnittger Institut de Biologie Mol�culaire des Plantes du CNRS, IBMP-CNRS - UPR2357 Strasbourg FRANCE Details: "Toward Deciphering the Network Architecture of Cyclin-Dependent Kinase Action" ABSTRACT Cyclin-dependent kinases are the central regulators of the cell cycle and as such key to growth, development and reproduction. The function of CDKs is conserved from yeast to plants and for example, expression of CDKA;1, the plant Cdk1 homolog, can complement yeast cdc2 or Cdc28 mutants. In addition, recent studies have shown that the molecular mechanistics of Cdk1-like kinases are conserved across kingdoms, e.g. the requirement for its activation through phosphorylation of a conserved Thr residue in their T-loop. In contrast to the conserved enzymatic function, the regulatory network of their action appears to have undergone dramatic changes during two billion years of eukaryotic evolution. This is illustrated by the recent finding that a Cdc25-Wee1 regulatory module is absent in the flowering plant Arabidopsis. Through extensive studies in yeast and humans, a comprehensive picture of CDK function has been revealed. We are interested in the properties of the network architecture of CDK action to understand general principles of cellular organization and coordination by cell-cycle control. As a starting point, we are following three complementing approaches to identify CDKA;1 substrates in Arabidopsis as a eukaryote very distantly related to metazoans and yeast. First, we exploit a modified bimolecular complementation assays to identify kinase substrates. Second, we have generated a gatekeeper mutant of CDKA;1 that can rescue cdka;1 mutants. In the gatekeeper variant the ATP binding pocket is mutated in such a way that bulky derivatives of ATP can be accepted by the kinase allowing the identification of proteins that were phosphorylated by this kinase variant. Third, we are analyzing the phospho-proteome of weak-loss-of-function mutants of CDKA;1. These approaches are providing a growing list of putative CDKA;1 substrates in Arabidopsis. Here, I will give a progress report of our current attempts and compare the so far identified substrates with data from yeast and humans.

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PSB event reminder
by contact＠psb.vib-ugent.be 04 Jan '11

04 Jan '11

Calendar Name: seminars Scheduled for: Thursday, January 6 2011, 11:00 - 12:30 Event text: Dr Arp Schnittger Institut de Biologie Mol�culaire des Plantes du CNRS, IBMP-CNRS - UPR2357 Strasbourg FRANCE Details: "Toward Deciphering the Network Architecture of Cyclin-Dependent Kinase Action" ABSTRACT Cyclin-dependent kinases are the central regulators of the cell cycle and as such key to growth, development and reproduction. The function of CDKs is conserved from yeast to plants and for example, expression of CDKA;1, the plant Cdk1 homolog, can complement yeast cdc2 or Cdc28 mutants. In addition, recent studies have shown that the molecular mechanistics of Cdk1-like kinases are conserved across kingdoms, e.g. the requirement for its activation through phosphorylation of a conserved Thr residue in their T-loop. In contrast to the conserved enzymatic function, the regulatory network of their action appears to have undergone dramatic changes during two billion years of eukaryotic evolution. This is illustrated by the recent finding that a Cdc25-Wee1 regulatory module is absent in the flowering plant Arabidopsis. Through extensive studies in yeast and humans, a comprehensive picture of CDK function has been revealed. We are interested in the properties of the network architecture of CDK action to understand general principles of cellular organization and coordination by cell-cycle control. As a starting point, we are following three complementing approaches to identify CDKA;1 substrates in Arabidopsis as a eukaryote very distantly related to metazoans and yeast. First, we exploit a modified bimolecular complementation assays to identify kinase substrates. Second, we have generated a gatekeeper mutant of CDKA;1 that can rescue cdka;1 mutants. In the gatekeeper variant the ATP binding pocket is mutated in such a way that bulky derivatives of ATP can be accepted by the kinase allowing the identification of proteins that were phosphorylated by this kinase variant. Third, we are analyzing the phospho-proteome of weak-loss-of-function mutants of CDKA;1. These approaches are providing a growing list of putative CDKA;1 substrates in Arabidopsis. Here, I will give a progress report of our current attempts and compare the so far identified substrates with data from yeast and humans.

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seminar Dr Wim Soppe 20/01/11
by Nathalie Vanden Hautte 21 Dec '10

21 Dec '10

You are receiving this e-mail because you subscribed to our seminars announcements and reminders service at https://maillist.psb.ugent.be/mailman/listinfo/seminars <https://maillist.psb.ugent.be/mailman/listinfo/seminars> . If you do not wish to receive this information anymore, please unsubscribe from future mailings at https://maillist.psb.ugent.be/mailman/options/seminars <https://maillist.psb.ugent.be/mailman/options/seminars> . VIB - Department of Plant Systems Biology Technologiepark 927 B - 9052 Gent/Zwijnaarde Phone: +32 9 33 13 800 Fax: +32 9 33 13 809 Http://www.psb.vib-ugent.be

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seminar Dr Arp Schnittger
by Nathalie Vanden Hautte 21 Dec '10

21 Dec '10

You are receiving this e-mail because you subscribed to our seminars announcements and reminders service at https://maillist.psb.ugent.be/mailman/listinfo/seminars <https://maillist.psb.ugent.be/mailman/listinfo/seminars> . If you do not wish to receive this information anymore, please unsubscribe from future mailings at https://maillist.psb.ugent.be/mailman/options/seminars <https://maillist.psb.ugent.be/mailman/options/seminars> . VIB - Department of Plant Systems Biology Technologiepark 927 B - 9052 Gent/Zwijnaarde Phone: +32 9 33 13 800 Fax: +32 9 33 13 809 Http://www.psb.vib-ugent.be

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upcoming seminars January
by Nathalie Vanden Hautte 21 Dec '10

21 Dec '10

Dear All Enclosed you can find our upcoming seminars for January. Kind regards Nathalie ____________________________________________ Nathalie Vanden Hautte Administrative Assistant VIB, Department of Plant Systems Biology Ghent University Technologiepark 927 9052 Gent Belgium Phone: +32/9/33.13.800 Fax: +32/33.13.809 Http://www.psb.ugent.be nahau(a)psb.vib-ugent.be

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PSB event reminder
by contact＠psb.vib-ugent.be 17 Dec '10

17 Dec '10

Calendar Name: seminars Scheduled for: Friday, December 17 2010, 11:00 - 12:30 Event text: Alexis Maizel Department of Stem Cell Biology Center for organismal studies University of Heidelberg Heidelberg GERMANY Details: "Control of developmental plasticity and robustness by small RNAs in Arabidopsis" ABSTRACT Plants adapt to their environment by forming new organs throughout their entire postembryonic life. The harmonious growth of these organs in response to morphogenetic signals is essential. Lateral roots unceasingly branch from the main root in response to local auxin maxima. How a local maximum translates to a robust pattern of gene activation ensuring the proper growth of the newly formed root is not known. The TAS3-derived trans-acting siRNAs (ta-siRNAs) belong to a plant-specific class of endogenous small RNAs, whose biogenesis requires the initial microRNA 390 (miR390)-mediated cleavage of the TAS3 precursor by AGO7. The ta-siRNAs target mRNAs encoding ARF3/ETTIN and ARF4 which are transcription factors of the AUXIN RESPONSE FACTORs that mediate the effects of auxin. I will present recent results establishing that auxin maxima at the sites of lateral root initiation promote localised production of miR390, allowing the formation of ta-siARFs to subsequently inhibit ARF3/4 activity in the incipient primordia. In turn, ARF3 and ARF4 contribute both positively and negatively to miR390 accumulation. These results support a model in which small RNAs employ target genes to regulate their own production.

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