Mini-courses

Aging and neurodegeneration: the role of redox processes and DNA repair mechanisms
Redox process can culminate in genomic instability that is strict related with the aging process as well as with aging-related neurodegenerative diseases. Thus, during the course we are going to discuss the role of the redox processes in DNA damage, DNA repair, mutagenesis, senescence and cellular death. Moreover, we are going to discuss how those lesions can lead to aging and to neurodegenerative diseases.


DNA lesions and repair in host-pathogen interaction
Pathological processes such as bacterial, viral and parasitic infections are able to generate oxidative stress, in which result can be harmful to host and/or pathogen. This stress occurs when there is an imbalance between reactive oxygen species produced and antioxidant factors produced in response to the infection. This imbalance can lead to DNA lesions of both infected cells and pathogen. The course will discuss the survival strategies developed by host cells and trypanosomatid pathogens focusing on the DNA repair mechanisms of these organisms throughout infection.


Mitochondrial DNA repair
Mitochondria are unique in animal cells in the sense that they are the only organelles that contain their own genome, reminiscent of their bacterial origin. In humans, the mitochondrial genome is a closed circular molecule of 16.5 kb, which encodes 13 polypeptides, 2 rRNAs and 22 tRNAs. All 13 polypeptides encoded in the mtDNA are subunits of the oxidative phosphorylation complexes and are essential for mitochondrial function and ATP generation. Thus, damage to the mtDNA may have severe functional consequences. Although initially thought to be devoid of DNA repair activities, mammalian mitochondria are proficient in repairing several types of DNA damage. In this course, we present the DNA repair pathways and discuss the similarities and differences between nuclear and mitochondrial DNA repair, with emphasis on their roles in maintaining mtDNA stability and mitochondrial function.