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The outcome of their research on viral strategies that affect cellular
functions has recently been published.
For several years, Professor Margarita Salas from the CBMSO has
dedicated part of her research efforts to the study of the replication
mechanism of virus 29, which infects the Bacillus subtilis, harmless
bacteria commonly found in the soil. Her work has contributed towards
a better understanding of the interactions between the viruses and
their target cells at a molecular level. In an article published last
year in the Journal of Biological Chemistry (Vol. 281: 7068-7074;
2006), Professor Salas and her team described an important discovery:
the protein p56 of virus 29 inhibits the activity of the cellular
protein uracil-DNA-glycosylase (UDG). It is known that this enzyme,
present in all living organisms, is involved in the DNA repair
processes and hence, it avoids mutations in the cellular genome.
In order to carry out its function, the UDG enzyme first identifies
the damaged DNA by locating uracil residues and then attaches itself
to the DNA to repair it. Recently, Professor Salas team, in
collaboration with the research group managed by Professor Manuel
Espinosa from the CIB, have published their new discoveries in Nucleic
Acids Research (Vol. 35: 5393-5401; 2007), recounting how the viral
protein p56 manages to inhibit the activity of the UDG enzyme. Their
experiments show that the protein p56 conceals the part of the UDG
enzyme that interacts with the damaged DNA so that there is no
possibility of attachment.
The protein p56 might accomplish this by imitating the structural
characteristics of DNA in order to mislead the UDG enzyme. If the
theory is corroborated, this would be another case of molecular
mimesis as an enzyme inhibitor technique. The future work by Professor
Salas and her team will be dedicated to substantiating this hypothesis.
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