News

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.

By directly altering the gene coding for the prion protein (PrP), Whitehead Institute researchers have created mouse models of two neurodegenerative prion diseases, each of which manifests in different regions of the brain.  These new models for fatal familial insomnia (FFI) and Creutzfeldt-Jakob disease (CJD) accurately reflect the distinct patterns of destruction caused by the these diseases in humans.  Remarkably, as different as each disease is, they both spontaneously generate infectious prions.

By studying the planarian flatworm, a master of regenerating missing tissue and repairing wounds, the lab of Whitehead Institute Member Peter Reddien has identified an unexpected source of position instruction: the muscle cells in the planarian body wall. This is the first time that such a positional control system has been identified in adult regenerative animals.

By tracking the previously unknown movements of a set of specialized cells, Whitehead Institute scientists are shedding new light on how the immune system mounts a successful defense against hostile, ever-changing invaders.