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Showing 31 to 33 of 33 (0.033 seconds)Spelling suggestions: "subject:"zip"" "subject:"bip""
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EXPLORING THE MOLECULAR MECHANISM OF ROOT-MEDIATED RESPONSES TO <i>RALSTONIA</i>Katherine Rivera-Zuluaga (17552421) 06 December 2023 (has links)
<p dir="ltr">Bacterial Wilt, caused by <i>Ralstonia solanacearum</i>, is among the most devastating plant diseases in the world. This pathogen causes significant loss in crops such as tobacco, potato, and tomato. <i>R. solanacearum</i> root infection and xylem colonization determine disease outcome. To date, little is known about the defense mechanism mediated by roots to prevent <i>R. solanacearum</i> vascular colonization during the initial infection stages. Plant early responses are important since they may impact disease outcomes<i>.</i><i> </i>Here, we report the formation of root hairs and primary root growth inhibition in tomato seedlings as <i>Ralstonia</i>-induced phenotypes that depend on tomato genotype and <i>Ralstonia</i> species. The <i>Ralstonia</i>-induced root phenotypes are independent of a functional type III secretion system and exopolysaccharide production (EPS). We also found that <i>R. solanacearum</i><i> </i>K60 infection increased auxin levels throughout the root meristem in wilt-susceptible tomato roots. Our data suggest proper auxin signaling and transport are important for susceptibility to <i>R. solanacearum</i> K60. Blocking auxin transport pharmacologically or genetically led to fewer wilting symptoms, suggesting that auxin is important during early infection stages and disease outcomes in tomato. We previously found that a tomato mutant defective in auxin transport and signaling, known as <i>diageotropica</i> (<i>dgt</i>), has enhanced resistance to <i>R. solanacearum</i> K60. We characterized the resistant response in the <i>dgt</i> mutant, and we found that the resistant response in the <i>dgt</i> mutant may be due to increased lignin content preventing pathogen vasculature colonization. <i>DGT</i> encodes a cyclophilin protein that regulates auxin transport and signaling. Mutations in the cyclophilin DGT promote resistance to <i>R. solanacearum</i> K60. DGT has been reported to regulate auxin transport and signaling. However, the molecular mechanism regarding how DGT mediates these processes is still unknown. We used Yeast Two-Hybrid to identify candidate protein interactors, and we found that SlbZIP1/SlbZIP29, Sl14-3-3, and SlMYB110 may interact with DGT to regulate both development and defense responses. Understanding the role of DGT, auxin, and lignin in defense responses to <i>R. solanacearum</i> K60 in tomato is necessary for Solanaceae crop improvement.</p>
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The Rtg1 and Rtg3 proteins are novel transcription factors regulated by the yeast hog1 mapk upon osmotic stressNoriega Esteban, Núria 27 February 2009 (has links)
La adaptación de la levadura Saccharomyces cerevisiae a condiciones de alta osmolaridad está mediada por la vía de HOG ((high-osmolarity glycerol). La activación de esta vía induce una serie de respuestas que van a permitir la supervivencia celular en respuesta a estrés. La regulación génica constituye una respuesta clave para dicha supervivencia. Se han descrito cinco factores de transcripción regulados por Hog1 en respuesta a estrés osmótico. Sin embargo, éstos no pueden explicar la totalidad de los genes regulados por la MAPK Hog1. En el presente trabajo describimos cómo el complejo transcripcional formado por las proteínas Rtg1 y Rtg3 regula, a través de la quinasa Hog1, la expresión de un conjunto específico de genes. Hog1 fosforila Rtg1 y Rtg3, aunque ninguna de estas fosforilaciones son esenciales para regulación transcripcional en respuesta a estrés. Este trabajo también muestra cómo la deleción de proteínas RTG provoca osmosensibilidad celular, lo que indica que la integridad de la vía de RTG es esencial para la supervivencia celular frente a un estrés osmótico. / In Saccharomyces cerevisiae the adaptation to high osmolarity is mediated by the HOG (high-osmolarity glycerol) pathway, which elicits different cellular responses required for cell survival upon osmostress. Regulation of gene expression is a major adaptative response required for cell survival in response to osmotic stress. At least five transcription factors have been reported to be controlled by the Hog1 MAPK. However, they cannot account for the regulation of all of the genes under the control of the Hog1 MAPK. Here we show that the Rtg1/3 transcriptional complex regulates the expression of specific genes upon osmostress in a Hog1-dependent manner. Hog1 phosphorylates both Rtg1 and Rtg3 proteins. However, none of these phosphorylations are essential for the transcriptional regulation upon osmostress. Here we also show that the deletion of RTG proteins leads to osmosensitivity at high osmolarity, suggesting that the RTG-pathway integrity is essential for cell survival upon stress.
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SCF cdc4 regulates msn2 and msn4 dependent gene expression to counteract hog1 induced lethalityVendrell Arasa, Alexandre 16 January 2009 (has links)
L'activació sostinguda de Hog1 porta a una inhibició del creixement cel·lular. En aquest treball, hem observat que el fenotip de letalitat causat per l'activació sostinguda de Hog1 és parcialment inhibida per la mutació del complexe SCFCDC4. La inhibició de la mort causada per l'activació sostinguda de Hog1 depèn de la via d'extensió de la vida. Quan Hog1 s'activa de manera sostinguda, la mutació al complexe SCFCDC4 fa que augmenti l'expressió gènica depenent de Msn2 i Msn4 que condueix a una sobreexpressió del gen PNC1 i a una hiperactivació de la deacetilassa Sir2. La hiperactivació de Sir2 és capaç d'inhibir la mort causada per l'activació sostinguda de Hog1. També hem observat que la mort cel·lular causada per l'activació sostinguda de Hog1 és deguda a una inducció d'apoptosi. L'apoptosi induïda per Hog1 és inhibida per la mutació al complexe SCFCDC4. Per tant, la via d'extensió de la vida és capaç de prevenir l'apoptosi a través d'un mecanisme desconegut. / Sustained Hog1 activation leads to an inhibition of cell growth. In this work, we have observed that the lethal phenotype caused by sustained Hog1 activation is prevented by SCFCDC4 mutants. The prevention of Hog1-induced cell death by SCFCDC4 mutation depends on the lifespan extension pathway. Upon sustained Hog1 activation, SCFCDC4 mutation increases Msn2 and Msn4 dependent gene expression that leads to a PNC1 overexpression and a Sir2 deacetylase hyperactivation. Then, hyperactivation of Sir2 is able to prevent cell death caused by sustained Hog1 activation. We have also observed that cell death upon sustained Hog1 activation is due to an induction of apoptosis. The apoptosis induced by Hog1 is decreased by SCFCDC4 mutation. Therefore, lifespan extension pathway is able to prevent apoptosis by an unknown mechanism.
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