Renowned developmental biologist Tatjana Piotrowski, Ph.D., and trailblazing regeneration expert Alejandro Sánchez Alvarado, Ph.D., joined the Stowers Institute for Medical Research, the Institute announced today.
A report from the Conaway lab at the Stowers Institute for Medical Research in the July 8, 2011, edition of the journal Cell identifies a switch that allows RNA polymerase to shift gears from neutral into drive and start transcribing. This work sheds light on a process fundamental to all plant or animal cells and suggests how transcriptional anomalies could give rise to tumors.
Stowers researchers pinpoint the Super Elongation Complex as a major regulator in the coordinated expression of early developmental genes.
Successful gene expression requires the concerted action of a host of regulatory factors. Long overshadowed by bonafide transcription factors, coactivators—the hanger-ons that facilitate transcription by docking onto transcription factors or modifying chromatin—have recently come to the fore.
Our bodies are perfectly capable of renewing billions of cells every day but fail miserably when it comes to replacing damaged organs such as kidneys. Using the flatworm Schmidtea mediterranea—famous for its capacity to regrow complete animals from minuscule flecks of tissue—as an eloquent example, researchers at the Stowers Institute for Medical Research demonstrated how our distant evolutionary cousins regenerate their excretory systems from scratch.
Most cells rely on structural tethers to position chromosomes in preparation for cell division. Not so oocytes. Instead, a powerful intracellular stream pushes chromosomes far-off the center in preparation for the highly asymmetric cell division that completes oocyte maturation upon fertilization of the egg, report researchers at the Stowers Institute for Medical Research.
All stem cells—regardless of their source—share the remarkable capability to replenish themselves by undergoing self-renewal. Yet, so far, efforts to grow and expand scarce hematopoietic (or blood-forming) stem cells in culture for therapeutic applications have been met with limited success.
After more than a century of study, mysteries still remain about the process of meiosis—a special type of cell division that helps insure genetic diversity in sexually-reproducing organisms. Now, researchers at Stowers Institute for Medical Research shed light on an early and critical step in meiosis.
Each time a cell divides—and it takes millions of cell divisions to create a fully grown human body from a single fertilized cell—its chromosomes have to be accurately divvied up between both daughter cells. Researchers at the Stowers Institute for Medical Research used, ironically enough, the single-celled organism Saccharomyces cerevisiae—commonly known as baker’s yeast—to gain new insight into the process by which chromosomes are physically segregated during cell division.
The accumulation of damaged protein is a hallmark of aging that not even the humble baker’s yeast can escape. Yet, aged yeast cells spawn off youthful daughter cells without any of the telltale protein clumps. Now, researchers at the Stowers Institute for Medical Research may have found an explanation for the observed asymmetrical distribution of damaged proteins between mothers and their youthful daughters.
The trifecta of biological proof is to take a discovery made in a simple model organism like baker’s yeast and track down its analogs or homologs in “higher” creatures right up the complexity scale to people, in this case, from yeast to fruit flies to humans. In a pair of related studies, scientists at the Stowers Institute for Medical Research have hit such a trifecta, closing a circle of inquiry that they opened over a decade ago.
Transcriptional elongation control takes on new dimensions as Stowers researchers find gene class-specific elongation factors.
Researchers at the University of California, San Francisco and the Stowers Institute for Medical Research have discovered that planarians, tiny flatworms fabled for their regenerative powers, completely lack centrosomes, cellular structures that organize the network of microtubules that pulls chromosomes apart during cell division.
Stress-induced genomic instability facilitates rapid cellular adaption in yeast.
Stowers researchers discovered that a prion-like protein plays a key role in storing long-term memories.
In a standard biology textbook, cells tend to look more or less the same from all sides. But in real life cells have fronts and backs, tops and bottoms, and they orient many of their structures according to this polarity explaining, for example, why yeast cells bud at one end and not the other.
Just like a road atlas faithfully maps real-word locations, our brain maps many aspects of our physical world: Sensory inputs from our fingers are mapped next to each other in the somatosensory cortex; the auditory system is organized by sound frequency. The olfactory system was believed to map similarly, where groups of chemically related odorants - amines, ketones, or esters, for example - register with clusters of cells that are laid out next to each other.
Few molecules are more interesting than DNA—except of course RNA. After two decades of research, that “other macromolecule” is no longer considered a mere messenger between glamorous DNA and protein-synthesizing machines. We now know that RNA has been leading a secret life, regulating gene expression and partnering with proteins to form catalytic ribonucleoprotein (RNP) complexes.
Cells on the move reach forward with lamellipodia and filopodia, cytoplasmic sheets and rods supported by branched networks or tight bundles of actin filaments. Cells without functional lamellipodia are still highly motile but lose their ability to stay on track, report researchers at the Stowers Institute for Medical Research in the April 9, 2012, online issue of the Journal of Cell Biology.
A team of Stowers scientists defines biochemical crosstalk between DNA interacting proteins and their modifications.
Stowers scientists use fruit flies to reveal unknown function of a transcriptional regulator of development and cancer
An actin-ratchet tightens the contractile ring that severs budding daughter cells from their yeast mothers.
“Paper of the week” shows that a master regulator protein brings plethora of coactivators to gene expression sites.
Non-canonical Wnt-signaling maintains a quiescent pool of blood-forming stem cells in mouse bone marrow.
Stowers team reconciles puzzling findings relating to centromere structure.
Stowers scientists make a surprising find in study of sex- and aggression-triggering vomeronasal organ.
Stowers scientists manipulate the Set2 pathway to show how genes are faithfully copied.
Researchers show how repressor proteins ensure accurate gene expression by thwarting histone exchange.
Stowers investigators define factors that regulate size of cellular fat pools.
Stowers scientists show how pluripotent stem cells mobilize in wounded planarian worms, to better understand stem cell behavior in regeneration and disease.
Changes in how DNA interacts with histones—the proteins that package DNA—regulate many fundamental cell activities from stem cells maturing into a specific body cell type or blood cells becoming leukemic. These interactions are governed by a biochemical tug of war between repressors and activators, which chemically modify histones signaling them to clamp down tighter on DNA or move aside and allow a gene to be expressed.
Chromatin remodeling—the packaging and unpackaging of genomic DNA and its associated proteins—regulates a host of fundamental cellular processes including gene transcription, DNA repair, programmed cell death as well as cell fate. In their latest study, scientists at the Stowers Institute for Medical Research are continuing to unravel the finicky details of how these architectural alterations are controlled.
New paper in Cell Reports finds that one key mechanism in development involves ‘paused’ RNA polymerase.
Unlike less versatile muscle or nerve cells, embryonic stem cells are by definition equipped to assume any cellular role. Scientists call this flexibility “pluripotency,” meaning that as an organism develops, stem cells must be ready at a moment’s notice to activate highly diverse gene expression programs used to turn them into blood, brain, or kidney cells.
Genetic analysis by Stowers investigators has implications for a genetic disorder known as Hirschsprung Syndrome.
A better “mousetrap” discovered in fruit flies might stop a human cancer-driving kinase in its tracks.
Study of tentacle-formation in a sea anemone shows how epithelial cells form elongated structures and puts the spotlight on a new model organism.
Stowers Institute Investigator Peter Baumann, Ph.D., has been appointed to the prestigious position of Howard Hughes Medical Institute (HHMI) investigator.
Stowers investigators discover how an unusual interplay of signaling pathways shapes a critical eye structure
Genomic imprinting maintains a reserve pool of blood-forming stem cells in mouse bone marrow
Stowers investigators use genetics and live cell imaging to illuminate molecular mechanisms that position the cell division machinery in growing tissues.
A little-studied factor known as the Little Elongation Complex (LEC) plays a critical and previously unknown role in the transcription of small nuclear RNAs (snRNA), according to a new study led by scientists at the Stowers Institute for Medical Research and published in the Aug. 22, 2013, issue of the journal Molecular Cell.
A decade ago, gene expression seemed so straightforward: genes were either switched on or off. Not both. Then in 2006, a blockbuster finding reported that developmentally regulated genes in mouse embryonic stem cells can have marks associated with both active and repressed genes, and that such genes, which were referred to as “bivalently marked genes”, can be committed to one way or another during development and differentiation.
When egg and sperm combine, the new embryo bustles with activity. Its cells multiply so rapidly they largely ignore their DNA, other than to copy it and to read just a few essential genes. The embryonic cells mainly rely on molecular instructions placed in the egg by its mother in the form of RNA.
Children born with developmental disorders called cohesinopathies can suffer severe consequences, including intellectual disabilities, limb shortening, craniofacial anomalies, and slowed growth. Researchers know which mutations underlie some cohesinopathies, but have developed little understanding of the downstream signals that are disrupted in these conditions.
The face you critiqued in the mirror this morning was sculpted before you were born by a transient population of cells called neural crest cells. Those cells spring from neural tissue of the brain and embryonic spinal cord and travel throughout the body, where they morph into highly specialized bone structures, cartilage, connective tissue, and nerve cells.
At a glance, DNA is a rather simple sequence of A, G, C, T bases, but once it is packaged by histone proteins into an amalgam called chromatin, a more complex picture emerges. Histones, which come in four subtypes—H2A, H2B, H3, and H4—can either coil DNA into inaccessible silent regions or untwist it to allow gene expression. To further complicate things, small chemical flags, such as methyl groups, affect whether histones silence or activate genes.
Disruptive clumps of mutated protein are often blamed for clogging cells and interfering with brain function in patients with the neurodegenerative diseases known as spinocerebellar ataxias. But a new study in fruit flies suggests that for at least one of these diseases, the defective proteins may not need to form clumps to do harm.
Prions can be notoriously destructive, spurring proteins to misfold and interfere with cellular function as they spread without control. New research, published in the open access journal PLOS Biology on February 11 2014, from scientists at the Stowers Institute for Medical Research reveals that certain prion-like proteins, however, can be precisely controlled so that they are generated only in a specific time and place. These prion-like proteins are not involved in disease processes; rather, they are essential for creating and maintaining long-term memories.
Researchers at the Stowers Institute for Medical Research have glimpsed two proteins working together inside living cells to facilitate communication between the cell's nucleus and its exterior compartment, the cytoplasm. The research provides new clues into how a crucial protein that is found in organisms from yeast to humans does its work.
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