Tag: Protein Function

Diagrams of DNA "goody bags"

Special chromosomal structures control key genes

October 7, 2014

Scientists have long theorized that the way in which the roughly three meters of DNA in a human cell is packaged to fit within a nuclear space just six microns wide, affects gene expression. Now, Whitehead Institute researchers present the first evidence that DNA structure does indeed have such effects—in this case finding a link between chromosome structure and the expression and repression of key genes.

Diagram of the Sestrins' role in mTORC1 regulation

New protein players found in key disease-related metabolic pathway

September 25, 2014

Cells rely on the mechanistic target of rapamycin complex 1 (mTORC1) pathway—which senses the availability of nutrients—to coordinate their growth with existing environmental conditions. The lab of Whitehead Member David Sabatini has identified a family of proteins that negatively regulate the branch upstream of mTORC1 that senses amino acids, the building blocks of proteins.

Images of tissue sections from breast cancer patient biopsies

Master heat-shock factor supports reprogramming of normal cells to enable tumor growth and metastasis

July 31, 2014

Long associated with enabling the proliferation of cancer cells, the ancient cellular survival response regulated by Heat-Shock Factor 1 (HSF1) can also turn neighboring cells in their environment into co-conspirators that support malignant progression and metastasis.

Graphic summary

Lost in translation? Not when it comes to control of gene expression during Drosophila development

May 29, 2014

The lab of Whitehead Member Terry Orr-Weaver has conducted perhaps the most comprehensive look yet at changes in translation and protein synthesis during a developmental change, using the oocyte-to-embryo transition in Drosophila as a model system. One of the insights from this research is that a surprisingly large number of mRNAs that are translationally regulated.

Schematic of how interrupting ATPIF1 rescues cells with mitochondrial dysfunction

Scientists find potential target for treating mitochondrial disorders

March 27, 2014

Mitochondria, long known as “cellular power plants” for their generation of the key energy source adenosine triphosphate (ATP), are essential for proper cellular functions. Mitochondrial defects are often observed in a variety of diseases, including cancer, Alzheimer’s disease, and Parkinson’s disease, and are the hallmarks of a number of untreatable genetic mitochondrial disorders whose manifestations range from muscle weakness to organ failure. Whitehead Institute scientists have identified a protein whose inhibition could hold the key to alleviating suffering caused by such disorders.

Image comparing a surface form and cave form of the fish Astyanax mexicanus

Rapid evolution of novel forms: Environmental change triggers inborn capacity for adaptation

December 12, 2013

A team of researchers from Harvard Medical School and Whitehead Institute report that, at least in the case of one variety of cavefish, one agent of evolutionary change is the heat shock protein known as HSP90.

Image showing how cells with and without normal FLCN gene react to nutrients

Gene responsible for hereditary cancer syndrome found to disrupt critical growth-regulating pathway

November 7, 2013

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.   

Microscope image of filamentation in Candida albicans with and without amphotericin B resistance

Understanding the evolution of drug resistance points to novel strategy for developing better antimicrobials

October 29, 2013

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.

Schematic showing nerve cells and person with Parkinson's disease within a yeast cell

Yeast, human stem cells drive discovery of new Parkinson’s disease drug targets

October 24, 2013

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.

Slides of mouse brain tissue from CJD mice that are infected with prions compared to tissue from FFI mice.

New models advance the study of deadly human prion diseases

August 19, 2013

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.

Thwarting protein production slows cancer cells’ malignant march

July 18, 2013

Protein production or translation is tightly coupled to a highly conserved stress response—the heat shock response and its primary regulator, heat shock factor 1 (HSF1)—that cancer cells rely on for survival and proliferation, according to Whitehead Institute researchers. In mouse models of cancer, therapeutic inhibition of translation interrupts HSF1’s activity, dramatically slowing tumor growth and potentially rendering drug-resistant tumors responsive to other therapies.

Image showing how a cell with a misaligned spindle corrects the problem

Bearing witness to the phenomenon of symmetric cell division

July 18, 2013

For more than 125 years, scientists have been peering through microscopes, carefully watching cells divide. Until now, however, none has actually seen how cells manage to divide precisely into two equally-sized daughter cells during mitosis. Such perfect division depends on the position of the mitotic spindle (chromosomes, microtubules, and spindle poles) within the cell, and it’s now clear that human cells employ two specific mechanisms during the portion of division known as anaphase to correct mitotic spindle positioning.

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