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New platform will help create designer human proteins in the lab

A group of researchers from Yale University and Agilent Technologies have developed a #syntheticbiology technique that turns bacterium E. Coli into a phosphorylated protein factory capable of churning out every known instance of this modification in human proteins.


Proteins, the end product of genes, carry out life functions. Most human proteins are modified by a process called serine phosphorylation — a chemical switch that can alter their structure and function. Malfunctions in this process have been implicated in diseases such as cancer and Alzheimer’s yet are difficult to detect and study. A group of researchers from Yale University and Agilent Technologies have developed a synthetic biology technique that turns bacterium E. Coli into a phosphorylated protein factory capable of churning out every known instance of this modification in human proteins.

“We synthesized over 110,000 phosphoproteins from scratch and we can now study how they all function together,” said Jesse Rinehart, associate professor of cellular and molecular physiology at the Systems Biology Institute and senior author of the research. “This is the future of scientific research — we can build everything we study.”

Previously, researchers were only able to create a single phosphoprotein at a time. The new platform will help scientists create designer proteins by studying the impact of phosphorylation on all potential protein interactions, the authors say. “Biologists want to know which proteins interact with each other because diseases can arise when these interactions go wrong,” said Karl Barber, a Yale graduate student who is the first author on the study and a recently named Schmidt Science Fellow.

The Limits of Neuroplasticity in the Brain

New research shows that the brain‘s neuroplasticity isn’t as flexible as previously thought.

One of the brain’s mysteries is how exactly it reorganizes new #information as you learn new tasks. The standard to date was to test how neurons learned new behavior one #neuron at a time.

Carnegie Mellon University and the University of Pittsburgh decided to try a different approach. They looked at the population of neurons to see how they worked together while #learning a new behavior. Studying the intracortical population activity in the primary motor cortex of rhesus macaques during short-term learning in a brain–computer interface (BCI) task, they were able to study the reorganization of population during learning.

Their new research indicates that when the brain learns a new activity that it is less flexible than previously thought. The researchers were able to draw strong hypothesis about neural reorganization during learning by using BCI. Through the use of BCI the mapping between #neural activity and learning is completely known

In this experimental paradigm, we’re able to track all of the neurons that can lead to behavioral improvements and look at how they all change simultaneously,” says Steve Chase, an associate professor of biomedical engineering at Carnegie Mellon and the Center for the Neural Basis of Cognition.

When we do that, what we see is a really constrained set of changes that happen, and it leads to this suboptimal improvement of performance. And so, that implies that there are limits that constrain how flexible your brain is, at least on these short time scales.”

It is often challenging to learn new tasks quickly that require a high level of proficiency. Neural plasticity is even more constrained than previously thought as results of this research indicate.

None of us predicted this outcome,” says Matthew Golub, a postdoctoral researcher in electrical and computer engineering at Carnegie Mellon. “Learning is far more limited on the scale of a few hours than any of us were expecting when we started this. We were all surprised that the brain wasn’t able to choose the best strategy possible.

The research was done in collaboration with the Center for Neural Basis of Cognition, a cross university research and educational program between Carnegie Mellon and the University of Pittsburgh that leverages each institution’s strengths to investigate the #cognitive and neural mechanisms that give rise to biological intelligence and behavior.

Nature Neuroscience (2018) Full Abstract Study

Aggregate form of α-synuclein leads to cell death in Parkinson’s Disease

An interaction between aggregate alpha synuclein and ATP synthase implicated in Parkinson’s Disease.


An open-access paper published in Nature Communications sheds light on how an accumulation of α-synuclein protein in brain cells contributes to causing Parkinson’s disease. In particular, the researchers discovered how clumps of the protein damage important proteins on mitochondrial surfaces, leading to impaired energy production, swelling and bursting of the mitochondria themselves, and, ultimately, cell death [1].

Study abstract

A Neuroscientist Explains What Happens to Your Brain When You Don’t Sleep

Sleep deprivation affects nearly all parts of your brain, but it is most detrimental to simple cognitive functions that we take for granted, such as memory and staying alert.

Ph.D. neuroscience candidate Shannon Odell says scientific research suggests that sleep deprivation majorly reduces cognitive performance. Studies have shown that patients have significantly reduced their thinking ability after just one night of sleep deprivation, specifically in the hippocampus, also known as the memory center.

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