Cellular response to stress and morphogenesis.
A precise coordination between cell proliferation and apoptosis is essential to maintain tissue homeostasis and to prevent tumor formation after DNA damage. Cells respond to this threat by arresting the cell cycle and activating the DNA repair mechanisms or by inducing apoptosis. These “life” vs “death” cell fate decisions are often regulated by the tumor suppressor gene p53. However, how the proliferating status of the cell can influence p53 cell fate decision making, is mostly unexplored. In this work, we address this important question by studying the apoptotic response after DNA damage in both experimentally arrested and endocycle-induced cells of the wing imaginal disc of Drosophila. The endocycle is of special interest as it is a modified cell cycle that alternates G and S phases without entering mitosis through the downregulation of Cdk1 activity.
In addition, we study the tumorigenic potential of p53 when its apoptotic role is inhibited. We find that cells with p53 that have inhibited its apoptotic potential acquire a persistent activity of the JNK pathway, which drives them into a senescent-like status and induce the non-autonomous overgrowth of the surrounding tissue.
The Master's student will acquire a strong background in genetics, molecular biology, and immunofluorescence techniques. Motivated students with strong curiosity and hardworking skills are encouraged to apply.
Carlos Estella.
Correo electrónico: cestella@cbm.csic.es.
Centro de Biología Molecular Severo Ochoa (CBM).
Número de plazas ofertadas: 1.
Facultad de Medicina. Universidad Autónoma de Madrid. Calle del Arzobispo Morcillo 4. 28029 Madrid. Tel.: +34 914 975 486. Correo electrónico: informacion.medicina@uam.es
