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Descripción
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| Plants have a postembryonic mode of development forming and growing new organs continuously. Plant postembryonic organogenesis requires new organs to be positioned and formed through the specification of organ founder cells and their subsequent development to generate new tissues. In Arabidopsis thaliana has been described that lateral root positioning is dependent on oscillating gene expression. Gene expression oscillations can be followed with the marker DR5, subsequently a static site of expression will be form, this marks the location where a new lateral root will be form (Moreno-Risueno et al., 2010) through the specification of a root organ founder cell. Out of an ethyl methanesulfonate screen, we identified a heritable mutation with altered postembryonic organogenesis, which we named potent. Stem cell and tissue specification is not affected in the main root of potent but the mutant does not produce lateral roots. We use lineage analyses and stem cell specification markers and found that new tissues are not specified in potent. To investigate defects in founder cell specification we focused on pericycle tissue because it is the tissue that is reprogrammed to generate lateral roots. In potent many pericycle cells present an altered identity, they do not present the marker J2661 that marks all pericycle cells, but however, they present the founder cell marker SKP2B. The founder cells in our mutant, although are normally arrested in subsequent development, can be stimulated to undergo organogenesis by auxin treatment, at a low auxin concentration that only induces the formation of lateral root from founder cells. We found that potent overproduces lateral roots. We mapped the mutation by next generation sequencing and we identify the affected gene, an Aux/IAA factor. The mutation is located in the domain that is involved in degradation of the protein upon auxin perception. We checked gene expression oscillations in our mutant detecting non-oscillating, almost continuous expression that could explain the elevated number of founder cells. When we checked more deeply potent pericycle we found regions where cells divided. However, they appeared to be divided symmetrically. We checked the marker MAKR4 that is expressed in the anticlinal membrane between two founder cell prior the nuclear migration that precede the asymmetric cell division and in the next divisions. The result in our mutant was that this marker was expressed in the anticlinal membrane of each pericycle cell or was not polarized. In addition, we observed that some divisions appear to be morphologically asymmetric in potent, however new cells show abnormal morphologies and no change in cell fate. These results suggest that our mutant may be involved in the correct polarization of founder cell to make a correct asymmetric cell division. | |
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Internacional
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No |
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Nombre congreso
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XIII Reunión de Biología Molecular de Plantas |
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Tipo de participación
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970 |
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Lugar del congreso
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Oviedo |
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Revisores
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ISBN o ISSN
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0000000000000 |
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DOI
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Fecha inicio congreso
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22/06/2016 |
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Fecha fin congreso
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24/06/2016 |
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Desde la página
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57 |
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Hasta la página
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57 |
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Título de las actas
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Libro de Resúmenes XIII Reunión de Biología Molecular de Plantas |