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Molecular & Cell Biology

Category: Molecular & Cell Biology

RNA polymerase II (Pol II), a key enzyme in our gene expression, is responsible for transcribing DNA into messenger RNA. Errors in transcription can cause deleterious effect upon repeated translation of erroneous mRNA into protein. Transcription infidelity may result in aging and human diseases such as cancer. During transcription, Pol II can detect the mis-incorporated RNA and backtrack to correct errors to ensure that each messenger RNA created will match with template DNA. However, it remains largely a mystery how Pol II controls the fidelity of gene transcription.

A microscope about the size of a penny is giving scientists a new window into the everyday activity of cells within the spinal cord. The innovative technology revealed that astrocytes--cells in the nervous system that do not conduct electrical signals and were traditionally viewed as merely supportive--unexpectedly react to intense sensation.

Scientists from Princeton University and Uppsala University in Sweden have identified a specific gene that within a year helped spur a permanent physical change in a finch species in response to a drought-induced food shortage. The findings provide a genetic basis for natural selection that, when combined with observational data, could serve as a comprehensive model of evolution.

A new study from the group of Holger Gerhardt (VIB/KU Leuven/Cancer Research UK/ MDC/BIH Berlin) in collaboration with Katie Bentley's Lab (Cancer Research UK/BIDMC-Harvard Medical School) addresses a long standing question in the wider field of developmental biology and tissue patterning in general, and in the vascular biology field in particular: 'What are the fundamental mechanisms controlling size and shape of tubular organ systems'. Whereas the most obvious way to grow a tube in size would be to add more building blocks (by proliferating cells) to enlarge its circumference, or to increase the size of the building blocks (the cells, hypertrophy), an alternative way would be to rearrange existing building blocks. Benedetta Ubezio, Raquel Blanco and colleagues under the direction of Holger Gerhardt and Katie Bentley now show that cell rearrangement is the way blood vessels switch from making new branches to increasing the size of a branch. The researchers also found that this switch is triggered by synchronization of cells under the influence of increasing levels of the growth factor VEGFA.

This is a skeletal preparation of a late stage skate embryo.
Latest analysis shows that human limbs share a genetic programme with the gills of cartilaginous fishes such as sharks and skates, providing evidence to support a century-old theory on the origin of limbs that had been widely discounted.

If genes form the body's blueprint, then the layer of epigenetics decides which parts of the plan get built. Unfortunately, many cancers hijack epigenetics to modulate the expression of genes, thus promoting cancer growth and survival. A team of researchers led by Tatiana Kutateladze, PhD, University of Colorado Cancer Center investigator and professor in the Department of Pharmacology at the University of Colorado School of Medicine, and Brian Strahl, PhD, professor in the Department of Biochemistry & Biophysics at the University of North Carolina School of Medicine, published a breakthrough report in the journal Nature Chemical Biology describing the essential role of YEATS domain proteins in reading epigenetic marks that regulate gene expression, DNA damage response, and other vital DNA-dependent cellular processes. This newly discovered player in epigenetic regulation is closely related to known cancer promoters, including the bromodomain proteins, a handful of which are targeted in current human clinical trials.

Scientists from Penn Medicine and other institutions unlock a mystery about 'long non-coding RNAs'.
A new genetic clue discovered by a team co-led by a researcher at the Perelman School of Medicine at the University of Pennsylvania is shedding light on the functions of the mysterious "long non-coding RNAs" (lncRNAs). These molecules are transcribed from genes and are often abundant in cells, yet they do not code for proteins. Their functions have been almost entirely unknown--and in recent years have attracted much research and debate.

The pace of evolution is typically measured in millions of years, as random, individual mutations accumulate over generations, but researchers at Cornell and Bar-Ilan Universities have uncovered a new mechanism for mutation in primates that is rapid, coordinated, and aggressive. The discovery raises questions about the accuracy of using the more typical mutation process as an estimate to date when two species diverged, as well as the extent to which this and related enzymes played a role in primate evolution.

A novel investigation of how enzymatic reactions can direct the motion and organization of microcapsules may point toward a new theory of how protocells - the earliest biological cells - could have organized into colonies and thus, could have ultimately formed larger, differentiated structures.

According to epigenetics -- the study of inheritable changes in gene expression not directly coded in our DNA -- our life experiences may be passed on to our children and our children's children. Studies on survivors of traumatic events have suggested that exposure to stress may indeed have lasting effects on subsequent generations. But how exactly are these genetic "memories" passed on?

Tardigrades have not acquired a significant proportion of their DNA from other organisms, a new study shows.
Tardigrades, also known as moss piglets or water bears, are eight-legged microscopic animals that have long fascinated scientists for their ability to survive extremes of temperature, pressure, lack of oxygen, and even radiation exposure.

Kent Bradford, left, and Alfred Huo, seen here with a flowering lettuce plant, found that lettuce could be prevented from flowering by increasing the expression of a specific microRNA
Like most annuals, lettuce plants live out their lives in quiet, three-act dramas that follow the seasons. Seed dormancy gives way to germination; the young plant emerges and grows; and finally in the climax of flowering, a new generation of seeds is produced. It's remarkably predictable, but the genetics that coordinates these changes with environmental cues has not been well understood.

Space-filling model of Reb1 bound to DNA.
In a study published on 28 March 2016 in the Proceedings of the National Academy of Sciences, researchers at the Medical University of South Carolina (MUSC) and Virginia Commonwealth University have resolved the first protein structure in a family of proteins called transcription terminators. The crystal structure of the protein, called Reb1, provides insight into aging and cancer, according to Deepak Bastia, Ph.D., Endowed Chair for Biomedical Research in the MUSC Department of Biochemistry and Molecular Biology and co-senior author of the study.

This image shows TFIID (blue) as it contacts the DNA and recruits the polymerase (grey) for gene transcription. The start of the gene is shown with a flash of light.
Your DNA governs more than just what color your eyes are and whether you can curl your tongue. Your genes contain instructions for making all your proteins, which your cells constantly need to keep you alive. But some key aspects of how that process works at the molecular level have been a bit of a mystery--until now.

Think your DNA is all human? Think again. And a new discovery suggests it's even less human than scientists previously thought.

Every cell on the surface of this genetically engineered zebrafish expresses a unique combination of green, red and blue fluorescent proteins, resulting in over 70 different hues
Scientists can now watch how hundreds of individual cells work together to maintain and regenerate skin tissue, thanks to a genetically engineered line of technicolor zebrafish.

When we remember events which occurred recently, the hippocampus is activated. This area in the temporal lobe of the brain is a hub for learning and memory. But what happens, if we try to remember things that took place years or decades ago? Neuroscientists at the Ruhr-University Bochum and the Osaka University have been able to give some answers to this question. They reveal that the neural networks involved in retrieving very old memories are quite distinct from those used to remember recent events. The results of the study have now been published in the open source science journal eLIFE.

Plants grown in high-density or crowded populations often put more energy into growth and maintenance than reproduction. For example, flowering may be delayed as plants allocate resources to growing taller and escape competition for light. This sensitivity to crowding stress has been observed in some varieties of sweet corn, but other varieties show higher tolerance, producing high yields even in crowded conditions. A recent University of Illinois and USDA Agricultural Research Service study attempted to uncover the genetic mechanisms of crowding tolerance in sweet corn.

This is the cover of Protein & Cell.
The human brain is extremely complex, containing billions of neurons forming trillions of synapses where thoughts, behavior and emotion arise. However, when an individual is performing a particular task, not many but only a few neural circuits are in action. The enormous cellular heterogeneity of the brain structure has made dissections of the molecular basis for neural circuitry function particularly challenging, because previous studies on genetic and epigenetic profiling using a block of brain tissues simply do not have the sufficient precision and accuracy to correspond to the activities of a few activated circuitries in the brain.

A new study out today in the journal Nature Communications shows that cells normally associated with protecting the brain from infection and injury also play an important role in rewiring the connections between nerve cells. While this discovery sheds new light on the mechanics of neuroplasticity, it could also help explain diseases like autism spectrum disorders, schizophrenia, and dementia, which may arise when this process breaks down and connections between brain cells are not formed or removed correctly.

This is an illustration of how the CRISPR/Cas system works, courtesy of Devaki Bhaya, Michelle Davison, and Rodolphe Barrangou.
You've probably seen news stories about the highly lauded, much-discussed genome editing system CRISPR/Cas9. But did you know the system was actually derived from bacteria, which use it to fight off foreign invaders such as viruses? It allows many bacteria to snip and store segments of DNA from an invading virus, which they can then use to "remember" and destroy DNA from similar invaders if they are encountered again. Recent work from a team of researchers including Carnegie's Devaki Bhaya demonstrates that some bacteria also use the CRISPR/Cas system to snip and recognize segments of RNA, not just DNA. It was published by Science.

GEMC1 is required for the generation of multiciliated cells. Images of mouse tracheas.
The genomic sequencing of hundreds of patients with diverse types of ciliopathies has revealed that "in many cases the gene responsible is not known", says Travis Stracker, head of the Genomic Instability and Cancer Lab at the IRB Barcelona. "So many people do not have a molecular diagnosis," stresses the researcher. "Our work seeks to contribute to bridging this knowledge gap".

HDAC5 (red) is a key factor in neurons for the control of food intake, astrocytes are stained in green.
Why do we get fat and why is it so difficult for so many people to keep off excess weight? Researchers in the Reseach Unit Neurobiology of Diabetes led by Dr. Paul Pfluger and at the Institute for Diabetes and Obesity led by Prof. Dr. Matthias Tschöp have now identified a new component in the complex fine-tuning of body weight and food intake. They found that the enzyme histone deacetylase 5 (HDAC5) has a significant influence on the effect of the hormone leptin*. This hormone plays a crucial role in triggering satiety and thus on how the body adapts to a changing food environment.

Left: Hexameric rings form a tube of viral capsid. Right: view from the other side of the protein oligomer.
Bank voles are small rodents that are not dangerous by themselves, but their excreta can contain one of the dangerous hantaviruses. While bank voles are unaffected by the infection, hantaviruses can cause potentially fatal diseases in humans for which no treatments exist. In central and northern Europe, infection is accompanied by fever, headache, or even renal failure. The strain that occurs in East Asia -- the Hantaan virus -- is even more dangerous: up to five percent of infected patients die of hemorrhagic fever, renal failure, or severe respiratory disorders.

__IMAGE_1 The mitochondrion isn't the bacterium it was in its prime, say two billion years ago. Since getting consumed by our common single-celled ancestor the "energy powerhouse" organelle has lost most of its 2,000+ genes, likely to the nucleus. There are still a handful left--depending on the organism--but the question is why. One explanation, say a mathematician and biologist who analyzed gene loss in mitochondria over evolutionary time, is that mitochondrial DNA is too important to encode inside the nucleus and has thus evolved to resist the damaging environment inside of the mitochondrion. Their study appears February 18 in Cell Systems.

Graphic of microtubules, the 'railway network' within every cell of the human body
Researchers from the University of Warwick have discovered how cells in the human body build their own 'railway networks', throwing light on how diseases such as bowel cancer work. The results have just been published in Nature Scientific Reports.

A new imaging technique has allowed researchers at North Carolina State University, the University of North Carolina at Chapel Hill, and the University of Pittsburgh to see how DNA loops around a protein that aids in the formation of a special structure in telomeres. The work provides new insights into the structure of telomeres and how they are maintained.

If you're fat, can you blame it on your genes? The answer is a qualified yes. Maybe. Under certain circumstances. Researchers are moving towards a better understanding of some of the roots of obesity.

Supposed "junk" DNA, found in between genes, plays a role in suppressing cancer, according to new research by Universities of Bath and Cambridge. The human genome contains around three metres of DNA, of which only about two per cent contains genes that code for proteins. Since the sequencing of the complete human genome in 2000, scientists have puzzled over the role of the remaining 98 per cent.

The scientists found that genome instability increases in cells as XPG levels decrease. The green spots mark locations of DNA double-strand breaks.
If you have a soft spot for unsung heroes, you'll love a DNA repair protein called XPG. Scientists from the U.S. Department of Energy's Lawrence Berkeley National Laboratory (Berkeley Lab) discovered that XPG plays a previously unknown and critical role helping to maintain genome stability in human cells. Their findings also raise the possibility that the protein helps prevent breast, ovarian, and other cancers associated with defective BRCA genes.

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