dSparc protege a las células de la eliminación por competición celular en Drosophila melanogaster

• Autores: Marta Portela Esteban
• Directores de la Tesis: Eduardo Moreno Lete (dir. tes.)
• Lectura: En la Universidad Autónoma de Madrid ( España ) en 2010
• Idioma: español
• Tribunal Calificador de la Tesis: Sonsoles Campuzano Corrales (presid.), Ernesto Sánchez-Herrero Arbide (secret.), Pedro P. López Casas (voc.), Florenci Serras Rigalt (voc.), Enrique Martín Blanco (voc.)
• Materias:
  • Ciencias de la vida
    • Biología molecular
• Enlaces
  • Tesis en acceso abierto en: Biblos-e Archivo
• Resumen

  • During cell life, cells accumulate mutations that can change their fitness.%&/Cell competition is a phenomenon that occurs among cells with different%&/metabolic rates. Cells with a proliferative advantage (winners) induce apoptosis%&/in loser cells and then displace them. Cell competition prevents the%&/accumulation of less fit cells and maintains cell number unchanged in tissues.%&/Field cancerization does not imply morphological alterations and seems to be%&/related with cell competition.%&/We have identified the Drosophila dSparc as an early marker%&/upregulated in loser cells. dSparc provides a transient shielding against cell-tocell%&/differences in cellular fitness, by setting a higher threshold for caspase%&/activation in loser cells. This mechanism may allow useful cells to recover from%&/transient and limited damage before they are unnecessarily eliminated by the%&/winners. If the differences in cellular fitness persist, cell competition induced%&/apoptosis is nevertheless triggered. dSparc expression might have a function in%&/restoring homeostasis in damaged tissues. Our models of cell competition%&/based in dMyc expression or stress allow us to study de function of dSparc in%&/cell competition.%&/Human homologue of dSparc has a variable expression in many tumors,%&/promoting tumour development, metastasis and field cancerization, in the other%&/hand, human dSparc also can act as a tumour suppressor. The reason of these%&/opposite functions remains unsolved. So, our work in Drosophila dSparc could%&/help to understand the dSparc role in human tumors.