Camps Laboratory: Where Cancer and Evolution Meet

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Manel Camps research group focuses on two biological questions: 1) Maintenance of genomic stability, i.e. how genetic information is preserved through accurate replication and through repair of DNA damage, and 2) Genetic adaptation, i.e. how random alterations in this information (mutations) drive the evolution of new biological activities. 

Maintenance of Genomic Stability: Our goal is to improve our mechanistic understanding of DNA repair, as a “gatekeeper” for genomic stability. Mutations obtained by directed evolution or that occur as natural polymorphisms are expressed in bacterial complementation systems to map the functional landscape of selected human DNA repair genes. Genomic instability increases the risk of cancer but is also used therapeutically, as it makes tumors hypersensitive to DNA damaging agents. We mine global transcriptome and drug sensitivity data to obtain additional clues as to how the different systems of DNA repair work together in a cell. This work will help customize antitumor therapy and should lead to the development of new approaches for cancer treatment.

Genetic Adaptation: We study how new biological activities arise during evolution using a combination of directed evolution and computational modeling. Our two main experimental systems are:

  1. The evolution in vitro of human DNA repair enzymes with altered specificity for N-methyl-, O-methyl, and etheno-DNA adducts to study structural determinants of substrate specificity
  2. The evolution of TEM-1 beta-lactamase mutants with extended-spectrum resistance to study how individual mutations combine to produce adaptive outcomes. This work has implications for rational protein design and for interpreting mutations associated with drug resistance, virulence, or genetic disease.

In addition, our group also pursues technology development.  Examples include genetic modulation of plasmid copy replication to facilitate recombinant protein expression and developing high-throughput screening methods to detect the introduction of random mutations by endogenous (polymerase errors) or exogenous (chemical mutagens) sources.

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