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The Research of Dr. Ivana De Domenico

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Molecular Biology

Promoting Safety In Biological Research

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As we prepare for a presidential election in November, the current administration is tackling an imperative undertaking: To set a way to govern potentially unsafe biological research trials that create infectious and lethal new germs.

According to an article published today on The Hill, researchers in 2011 reported tests that made deadly strains of influenza and the news raised worries that such novel infections could be purposely abused. Not to mention that there’ve been reports of lost smallpox vials at the National Institutes of Health, potential Bacillus anthracis exposures at the Centers for Disease Control, and different episodes at government labs highlighted wellbeing slips in even the nation’s top offices.

The White House will likely reveal a long haul strategy to solve this problem before January.

Writes The Hill’s Marc Lipsitch”

“The National Science Advisory Board on Biosecurity, charged to lead the deliberation, concluded that certain experiments – those with a high likelihood of producing novel, contagious and highly virulent infectious agents – are particularly worrisome and deserve special vetting for scientific necessity and safety before they are undertaken. The question is who should scrutinize them, and how.”

The US firmly limits perilous trials with germs and poisons that may entice weapons for bioterrorists. While this rule provides a structure with which to control experiments that make new fatal, transmissible infections, it’s still not fail-proof. “The Rule should be amended to prohibit the riskiest research that might produce highly virulent, contagious new strains of a pathogen, while permitting exceptions if an interagency expert panel judges the risk is warranted,” writes Lipsitch.

Replacement Bacterium for E.coli in Biological Research

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A new paper from Harvard presents an interesting development: The bacteriumVibrio natriegens grows considerably quicker than E. coli, which has been used for all manner of biological research from DNA studies to learning more about strains that make antibiotics.

What this could mean: Cutting down the time geneticists spend on routine investigations could, essentially, mean that researches could get twice as much research work done in the same amount of time if using the new bacterium.

Says Wired:

V. natriegens comes from the mud of a salt marsh, and it has a reputation as a speedy grower. It doubles in number every 10 minutes—compared to 20 minutes for E. coli in ideal growth conditions. But V. natriegens needs to do more than grow fast to be useful, and that’s where E. coli has the incumbent advantage. “Over the course of a hundred years of intense study, we have a huge amount of information about the organism, more than any other on Earth,” saysAdam Arkin, a biologist at the University of California, Berkeley, who was not involved in the study.

According to a study published by the American Society for Microbiology, V. natriegens is recognized as “one of the fastest-dividing organisms currently known, with a documented doubling time of 9.8 min (5). This is a growth rate that requires an extremely high rate of protein synthesis, which is accommodated by a higher rRNA gene dose, increases in ribosome numbers, strong rRNA promoters.”

Only time will tell whether this upstart of a microorganism will live up to its hype and significantly change the research landscape.

Smithsonian To Capture Genomic Diversity

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I found this interesting article that I thought I should share, which talks about the Smithsonian’s National Museum of Natural History’s plan to capture the genomic diversity of half the world’s living plant genera over the next two years. The Smithsonian will be partnering with the US Botanic Garden, the US Department of Agriculture’s US National Arboretum and the Global Genome Biodiversity Network.

The project comes at an extremely important time as the rate of species extinction for all life is estimated to be up to 100 times higher than normal, according to the Smithsonian. Global Genome Initiative Director Jonathan Coddington said that the project is looking “to preserve and unlock the genomic mysteries of plants.” This should certainly be an exciting project to follow over the next few years.

Scientists Find Molecule That Delays Alzheimer’s

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Alzheimer’s disease is one of the most debilitating and painful diseases that man has ever had the unfortunate chance to encounter. While there might be no pain for the person afflicted with it, the pain their family goes through as they watch the person they knew and loved become a shell is indescribable. While there has been decades of research into finding a cure for this terrible disease, it seems as though progress has never been made until now.

Scientists at the University of Cambridge have released a new study in Nature Structural & Molecular Biology that points to a victory in the long fight against alzheimer’s disease. Researchers have found that the onset of alzheimer’s can be delayed by a molecule that was found to occur naturally in the human brain. Studies in mice have already shown that this molecule puts a stop to many of the processes that lead to alzheimer’s and dementia. The molecule is called Brichos and while it won’t revert any damage that was already done, it will prevent any more damage from occurring.

One of the first signs of alzheimer’s is the formation of sticky clumps of proteins in the brain. Proteins, called amyloid betas, start folding in wrong shape and end up sticking together. These clumps continue to grow into fibers, called fibrils, and spread across the brain. Even though the brain has ways to deal with this sort of issue, it can quickly be overwhelmed and cause a chain reaction. The fibrils act like a catalyst for more clumps to form and the process is exponential as the disease progresses.

Brichos works by sticking to the amyloid fibrils, coating their exterior and preventing the formation of any more sticky clumps. Unfortunately, Brichos currently isn’t useful as a treatment source because it gets absorbed by the body too quickly to get an actual chance to work on the brain. However this discovery shows that the alzheimer’s process can be interrupted and that if we can find another molecule like Brichos then we have a real chance at stopping this tragic disease once and for all.

If you’d like to read more, the link is here.

Understanding LUCA

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All life forms have one common ancestor, in the form of a single-celled organism.  However, for centuries, the question of how this single-celled organism has evolved into the variety of life forms now evident has plagued biologists.  Research conducted by scientists at University College London can shed some light on the complex evolutions of this common ancestor, according to findings published in PLOS Biology and summarized in an article by Science Daily.

        The research focused on the evolution of Life’s Last Universal Common Ancestor, otherwise known as the LUCA.  The scientists built a model to monitor the changes in the membrane of the LUCA, in the hopes of examining how the ancestor is able to evolve into both bacteria and archaea—two types of single-celled organisms that have completely different cell membranes.

Luca tree
A visualization of groups of major organisms, and their relationship to the LUCA

        The model gave the LUCA a “leaky” membrane.  Through the inclusion of this leaky quality to the membrane, the LUCA was powered by energy driven from its surroundings, suggesting that the LUCA originally lived in areas with ancient seawater.  This seawater allowed protons, or positively charged particles, to mix with alkaline vent fluid.  From there, the leaky membrane enabled the protons to leave cell, allowing for more protons to enter the power growth; therefore, the LUCA was able to adapt and evolve, to escape the seabed vents.  In essence, the model showed all the steps the LUCA takes from being a strange cell to being the ancestor of all life today.  Through these steps, the team was able to observe how LUCA can evolve into both bacteria and archaea.

        In the future, the researchers, led by Victor Sojo, of the UCL CoMPLEX and Biosciences department and the first author of the study, hope to recreate the environment of the vents, as this is where it is believe life formed four billion years ago.

Role of Cyclin-D in Spread of Cancers

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Researchers at the University of California, San Diego School of Medicine have elucidated the role of a protein essential to regulating the progression of the cell cycle. Until recently, it assumed to promote development of cancer. Actually, it works to suppress the growth of tumors. Findings reported in the scientific journal eLife and recently covered by Science Daily show that cyclin-D, synthesized during the first stage of cell replication, is now believed to induce interactions with the retinoblastoma protein, otherwise known as Rb. Since we know that Rb acts as a tumor suppressor, mutilated and dysfunctional Rb is associated with several major cancers.

Scientists have long considered Cyclin-D has be a possible cause in the spread of cancer, as it hinders of the ability of Rb to suppress tumors through a process called phosphorylation. In the study, a team led by UC San Diego Department of Cellular and Molecular Medicine professor Steven F. Dowdy, took the effort to count the number of phosphates added to Rb during cell cycle progression. They began this process to discover how many single phosphates cyclin-D adds during the process. The results of their studies and observations found that cyclin-D adds one phosphate at one of the fourteen locations early along in the G1 phase of the cell cycle. This indicates that fourteen different versions of Rb tumor suppressors are created and instigated, thus enabling the activation of Rb.

The researchers believe these findings could change current understandings of the G1 cell cycle regulation, as well as the molecular origins of many of the common cancers affecting the general public today.

Fresh Findings about Relationship Between Regulation of DNA and Common Illnesses

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There’s a lot of major diseases out there that a one could suffer from. Once a patient acquires any of diseases, DNA wraps around specialized proteins called histones in the cell’s nucleus. The histones then work to keep DNA tightly packaged, preventing expression of genes and replication of DNA. This prevents the required cell growth that is evident in those who don’t suffer from some of the world’s most common diseases.

Researchers from the Faculty of Medicine and Dentistry at the University of Alberta have discovered a method of modifying and manipulating histones of the acetyl-group. They published their study and findings in the journal Cell, and it was subsequently reported by Science Daily. The researchers experimented with attaching a molecule called acetyl-CoA that enables relaxation of the DNA, allowing for a return of regular replication of DNA and gene expression. This mechanism, entitled “epigenetic regulation of DNA,” is crucial for normality of functions and in working against common diseases such as heart disease or cancer.

Image of a Nucleosome Model
A model of a nucleosome. The histones surfaces’ are blue; the DNA, yellow.

Department of Medicine postdoctoral fellows Gopinath Sutendra and professor Evangelos Michelakis led the team of researchers. Their ultimate findings grew to be even more detailed than anticipated, as the team also worked with an enzyme entitled Pyruvate Dehydrogenase Complex (PDC). This enzyme can find its way to the nucleus and work to generate the acetyl-CoA for histones. This particular finding shed light on the before unknown origins of acetyl-CoA in the nucleus.

According to the researchers, these findings will change strategies used in the war against cancer and other common diseases. The application of the findings in regards to how DNA is regulated could have larger implications as well, if future research aims to seek out further influences.