Research projects

Regeneration is the ability that allows organisms to repair or replace damaged tissues or structures. This capacity depends on different cellular processes that allow to re-establish the number and cell types that have been eliminated. Thus, during regeneration there are mechanisms that promote changes in cell specificity. The fact that these processes can be activated during regeneration suggests that there are genetic mechanisms that allow cell de-differentiation and reprogramming. Understanding how this process is regulated is crucial for developing new strategies to efficiently promote cell reprogramming. In our laboratory we use Drosophila melanogaster as a model system to define how this phenomenon is regulated. 

We have identified a previously unknown mechanim that imply the cooperative function  of JNK and JAK / STAT signalling pathways for inducing loss of cell fate specification.

 Another interesting unresolve problem is why regenerative capacity is lost as organisms develop or age. To answer this question it is necessary to obtain a better understanding of the genetic and cellular processes that limit regenerative capacity during development. Our results indicate that whereas the induction of damage in early stages of development produces an increase in proliferation through the activation of the cycle regulators CycE and E2f, in late stages only e2f is activated but not cycE. This would limit the ability of the cells to re-enter into the cell cycle and therefore to proliferate and  repair the damaged estructure. We have observed that the over-expression of cycE at the same time that damaged is induced  increases the proliferative capacity of cells in late stages of development These results suggest that in late stages of development the expression of CycE is blocked. This could be a limiting factor for the activation of regenerative proliferation and therefore it would be limiting regenerative capacity.