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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.

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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.

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Deploying sophisticated high-throughput sequencing technology, dubbed ψ-seq, a team of Whitehead Institute and Broad Institute researchers collaborated on a comprehensive, high-resolution mapping of ψ sites that confirms pseudouridylation, the most common post-transcriptional modification, does indeed occur naturally in mRNA.

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Induced pluripotent stem cells (iPSCs) can acquire serious genetic and epigenetic abnormalities that lower the cells’ quality and limit their therapeutic usefulness. Now Whitehead Institute researchers have identified a cocktail of reprogramming factors that produces very high quality iPSCs.

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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. implications for the diagnosis, prognosis, and management of cancer patients.

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A team of Whitehead Institute researchers is bringing new levels of efficiency and accuracy to one of the most essential albeit tedious tasks of bench science: pipetting. Dubbed “iPipet,” the system converts an iPad or any tablet computer into a “smart bench” that guides the execution of complex pipetting protocols.

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Embryonic stem cell (ESC) research has been hampered by the inability to transfer research and tools from mouse ESC studies to their human counterparts, in part because human ESCs are “primed” and slightly less plastic than the mouse cells. Now researchers in the lab of Whitehead Institute Founding Member Rudolf Jaenisch have discovered how to manipulate and maintain human ESCs into a “naïve” or base pluripotent state similar to that of mouse ESCs without the use of any reprogramming factors.

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A signaling pathway once thought to have little if any role during embryogenesis is a key player in the formation of the front-most portion of developing vertebrate embryos. Moreover, signals emanating from this region—referred to as the “extreme anterior domain” (EAD)—orchestrate the complex choreography that gives rise to proper facial structure.

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The protein CENP-A, which is integrated into human DNA at the centromere on each chromosome, has a vital role in cell division. Work from Whitehead Institute Member Iain Cheeseman’s lab describes how the vital and tightly controlled replenishment of CENP-A progresses.

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Whitehead Institute scientists have genetically and enzymatically modified red blood cells to carry a range of valuable payloads—from drugs, to vaccines, to imaging agents—for delivery to specific sites throughout the body.

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Metastatic cancer cells, which can migrate from primary tumors to seed new malignancies, have thus far been resistant to the current arsenal of anticancer drugs. Now, however, researchers at Whitehead Institute have identified a critical weakness that actually exploits one of these cells’ apparent strengths—their ability to move and invade tissues. Their research could inform novel approaches to screening tumors for personalized therapy or to drugs that specifically target these cells.

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In any animal’s lifecycle, the shift from egg cell to embryo is a critical juncture that requires a remarkably dynamic process that ultimately transforms a differentiated, committed oocyte to a totipotent cell capable of giving rise to any cell type in the body. The lab of Whitehead Member Terry Orr-Weaver 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.

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Whitehead Institute researchers have identified a potential dual-pronged approach to treating Niemann-Pick type C (NPC) disease, a rare but devastating genetic disorder. By studying nerve and liver cells grown from NPC patient-derived induced pluripotent stem cells (iPSCs), the scientists determined that although cholesterol does accumulate abnormally in the cells of NPC patients, a more significant problem may be defective autophagy—a basic cellular function that degrades and recycles unneeded or faulty molecules, components, or organelles in a cell.

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Whitehead Institute scientists have identified a genetic cause of a facial disorder known as hemifacial microsomia (HFM). The researchers find that duplication of the gene OTX2 induces HFM, the second-most common facial anomaly after cleft lip and palate.

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The lab of Whitehead Institute Member Peter Reddien is introducing the scientific community to the three-banded panther worm (Hofstenia miamia), a small organism with the ability to regenerate any missing body part. As a model, Hofstenia could help further our understanding of regeneration, how its mechanisms have evolved over millennia, and what limits regeneration in other animals, including humans. Intriguingly, Hofstenia and the planarian Schmidtea mediterranea—long the mainstay of Reddien’s research—rely on similar molecular pathways to control regeneration despite having evolved separately over the course of roughly 550 million years.

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The human Y chromosome has over the course of millions of years of evolution has preserved a small set of genes that has ensured not only its own survival but also the survival of men. Moreover, the vast majority of these tenacious genes appear to have little if any role in sex determination or sperm production. Taken together, these remarkable findings suggest that because these Y-linked genes are active across the body, they may actually be contributing to differences in disease susceptibility and severity observed between men and women.

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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.

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Whitehead Institute today announced it has entered into a scientific research collaboration with Biogen Idec (NASDAQ:BIIB) aimed at driving early stage research that may lead to the development of novel therapies across a broad range of disease areas.

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Scientists at Whitehead Institute have pinpointed a major mitochondrial pathway that imbues cancer cells with the ability to survive in low-glucose environments. By identifying cancer cells with defects in this pathway or with impaired glucose utilization, the scientists can predict which tumors will be sensitive to these anti-diabetic drugs known to inhibit this pathway.

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Whitehead Institute scientists have used a yeast cell-based drug screen to identify a class of molecules that target the amyloid-β (Aβ) peptide involved in Alzheimer’s disease (AD).

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Whitehead Institute researchers have determined that poly(A) tails on messenger RNAs (mRNAs) shift their role in the regulation of protein production during early embryogenesis. This finding about the regulation of mRNA translation also provides insight into how microRNAs control protein production.

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In this week’s edition of the journal Science, 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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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By creating a powerful new gene regulation system called CRISPR-on, Whitehead Institute researchers now have the ability to increase the expression of multiple genes simultaneously and precisely manipulate each gene’s expression level. The system is effective in both mouse and human cells as well as in mouse embryos.

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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.

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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.

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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.

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Painstaking new analysis of the genetic sequence of the X chromosome—long perceived as the “female” counterpart to the male-associated Y chromosome—reveals that large portions of the X have evolved to play a specialized role in sperm production.

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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.

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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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Whitehead Institute researchers have determined that the transcription factor Nanog, which plays a critical role in maintaining the self-renewal of embryonic stem cells, is expressed in a manner similar to other pluripotency markers. This finding contradicts the field’s presumptions about this important gene and its role in the differentiation of embryonic stem cells.

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Whitehead Institute researchers have determined that in basal breast cancer cells a transcription factor known as ZEB1 is held in a poised state, ready to increase the cells’ aggressiveness and enable them to transform into cancer stem cells capable of seeding new tumors throughout the body. Intriguingly, luminal breast cancer cells, which are associated with a much better clinical prognosis, carry this gene in a state in which it seems to be permanently shut down.

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Researchers at Whitehead Institute have identified a key target protein of glucocorticoids, the drugs that are used to increase red blood cell production in patients with certain types of anemia, including those resulting from trauma, sepsis, malaria, kidney dialysis, and chemotherapy. The discovery could spur development of drugs capable of increasing this protein’s production and thus increased numbers of red blood cells without causing the severe side effects associated with glucocorticoids.

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Whitehead Institute Founding Member Rudolf Jaenisch has efficiently created mouse models with multiple gene mutations in a matter of weeks. Because the method does not require embryonic stem cells, the approach also could allow any animal to become a model organism.

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In a surprising finding that helps explain fundamental behaviors of normal and diseased cells, Whitehead Institute scientists have discovered a set of powerful gene regulators dubbed “super-enhancers” that control cell state and identity.

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In the final year of the “Best Places to Work: Postdocs” ranking, Whitehead Institute has again come out on top. This is the fourth time in 10 years that Whitehead has emerged as number one—more than any other institution in the history of the rankings, published annually by The Scientist magazine.

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A team of scientists has added markedly to the job description of prions as agents of change, identifying a prion capable of triggering a transition in yeast from its conventional single-celled form to a cooperative, multicellular structure. This change, which appears to improve yeast’s chances for survival in the face of hostile environmental conditions, is an epigenetic phenomenon—a heritable alteration brought about without any change to the organism’s underlying genome.

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Whitehead Institute Founding Member Robert Weinberg is among 11 scientists to receive the new Breakthrough Prize in Life Sciences, intended to recognize excellence in research aimed at curing intractable diseases and extending human life.

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Whitehead Institute researchers report that 10 long noncoding RNAs (lncRNAs) play a vital role in the regulation of white fat cells. When each of these lncRNAs is individually knocked down, fat precursor cells fail to mature into white fat cells and have significantly reduced lipid droplets compared with white fat cells with unmodified lncRNA function.

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Research from Whitehead Institute shows that transcription at the active promoters of protein-coding genes commonly runs in opposite directions. This leads to coordinated production of both protein-coding messenger RNAs (mRNAs) and long noncoding RNAs (lncRNAs).

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Using only a computer, an Internet connection, and publicly accessible online resources, a team of Whitehead Institute researchers has been able to identify nearly 50 individuals who had submitted personal genetic material as participants in genomic studies.

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In an approach with the potential to aid therapeutic vaccine development, Whitehead Institute scientists have shown that enzymatically modified antibodies can be used to generate highly targeted, potent responses from cells of the immune system.

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One enzyme, RagA, has been found to regulate the mechanistic target of rapamycin complex 1 (mTORC1) pathway in cells according to glucose and amino acid availability. When this regulation breaks down in fasting newborn mice, the animals suffer a nutritional crisis and die.

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According to Whitehead Institute researchers, a protein known as monocarboxylate transporter 1 (MCT1), which is highly expressed in a subset of metabolically altered cancer cells, is needed for the entry of the investigational cancer drug 3-bromopyruvate (3-BrPA) into malignant cells.