By modifying the CRISPR-Cas genome editing system, Whitehead Institute researchers are now able to manipulate Candida albicans' genome systematically--an approach that could help identify novel targets for therapies against this serious pathogen for which there are a limited number of anti-fungal agents. "The ability to engineer Candida albicans with CRISPR technology has changed the playing field," says Whitehead Founding Member Dr. Gerald Fink, who is also a Professor of Biology at MIT. "We used to attack this human pathogen with our hands tied behind our back. Our findings cut these bonds, freeing us to forge ahead on problems in basic research and human health." C. albicans (image) is a commensal organism that normally lives harmlessly on the skin or in the gut. However, this yeast can grow in uncontrolled fashion--particularly in immunocompromised individuals--causing fungal infections ranging from mild to lethal. C. albicans is a hardy foe because many strains are resistant to anti-fungal drugs. To develop new anti-fungal agents, researchers need to know more about the organism’s basic biology. One tactic for identifying new drug targets in such pathogens is to knock out each of the organism's genes to determine which are essential and therefore appropriate as drug targets. The genome of C. albicans has been particularly difficult to crack because it has two copies of every gene and existing genome editing methods have been inefficient in knocking out both copies simultaneously. In 2012, a bacterial immunity system --the clustered, regularly interspaced, short palindromic repeats (CRISPR)-associated protein 9 (Cas) system--was repurposed for genome editing. It is precise and efficient enough to edit both copies of a gene in most diploid organisms. However, C.
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