News

Whitehead Institute scientists report that the gene mutated in the rare hereditary disorder known as Birt-Hogg-Dubé cancer syndrome prevents activation of mTORC1, a critical nutrient-sensing and growth-regulating cellular pathway.   

The most common fungal pathogen in humans, Candida albicans, rarely develops resistance to the antifungal drug amphotericin B (AmB).  This has been puzzling as the drug has been in clinical use for over 50 years. Whitehead Institute scientists have now discovered why.  The genetic mutations that enable certain strains of C. albicans to resist AmB simultaneously render it highly susceptible to environmental stressors and disarm its virulence factors.

Using a discovery platform whose components range from yeast cells to human stem cells, Whitehead Institute scientists have identified a novel Parkinson’s disease drug target and a compound capable of repairing neurons derived from Parkinson’s patients.

Revealing influenza’s truly insidious nature, Whitehead Institute scientists have discovered that the virus is able to infect its host by first killing off the cells of the immune system that are actually best equipped to neutralize the virus.

Having recently discovered a set of powerful gene regulators that control cell identity in a few mouse and human cell types, Whitehead Institute scientists are now showing that these regulators—which they named “super-enhancers”—act across a vast array of human cell types and are enriched in mutated regions of the genome that are closely associated with a broad spectrum of diseases.

Whitehead Institute researchers have discovered that the protein product of the gene MECP2, which is mutated in about 95% of Rett syndrome patients, is a global activator of neuronal gene expression. Mutations in the protein can cause decreased gene transcription, reduced protein synthesis, and severe defects in the AKT/mTOR signaling pathway.

Whitehead Fellows Sebastian Lourido and David Pincus have each been named a recipient of a 2013 National Institutes of Health (NIH) Director’s Early Independence Award, aimed at accelerating the careers of exceptionally creative junior scientists.

A new study from a team of Whitehead and MIT researchers reveals a gene that is critical to the process of memory extinction. Enhancing the activity of this gene, known as Tet1, might benefit people with posttraumatic stress disorder (PTSD) by making it easier to replace fearful memories with more positive associations.

By investigating regeneration in planarian flatworms, Whitehead Institute researchers have identified a mechanism—involving the interplay of two wound-induced genes—by which the animal can distinguish between wounds that require regeneration and those that do not.

Whitehead Institute researchers have used the gene regulation system CRISPR/Cas (for “clustered regularly interspaced short palindromic repeat/CRISPR-associated) to engineer mouse genomes containing reporter and conditional alleles in one step. Animals containing such sophisticated engineered alleles can now be made in a matter of weeks rather than years and could be used to model diseases and study gene function.