New study on an improved mouse model headed by researchers of The Ohio State University Wexner Medical Center, College of Medicine and Imperial College London discovered nerve cells’ capacity to regenerate and this might pave the way for new treatments of nerve damage.
As it was learned earlier, scientists looked at effects of the three-dimensional organisation of DNA in nerve cells in relation to their capacity to regenerate after an injury.
The structure revealed that particular DNA loops, known as promoter-enhancer loops, are essential for initiating the activation of genes that support regenerative growth of nerves. These loops are kept together by a protein known as cohesin After the DNA replication phase of the cell cycle the cohesin protein holds the sister chromatids together then releases them only when it is time for the cell to split.
The work was completed when Palmisano was at Imperial College London with co-investigator Professor Simone Di Giovanni, MD, Ph.D., in the Department of Brain Sciences at Imperial College and others including scientists at the University of Miami.
Chromatin is the manual or the instruction manual of each cell and it is tightly packed within a cell nucleus. How it ‘unfolds’ or ‘opens’ when switched on affects how the instructions are ‘read’ and integrated by the cells, Di Giovanni, who leads the study and is a Chair in Restorative Neuroscience at Imperial College, explained.
They had used mice in their previous works where they noted that diseases involving the existence of regenerative genes depend on the structure of chromatin. To cause the repair of injured nerves, the chromatin of neurons has to be open, according to Palmisano.
In today’s work conducted on mice, the team has found another part of chromatin’s structure that is essential for the treatment of injured nerves.
“It is understood that chromatin is folded into a multilayer structure in the form of three dimensional domains which are also a generic territory,” according to Palmisano. ‘These loops allow interaction between ‘genomic sites’ which are in fact located at a considerable distance from one another in the linear genomic map.’
Such contact points are critical for the following reason: they always facilitate communication between genes and enhancers – the regulatory sequences capable of increasing the activity of the genes in question.
It was discovered that upon injury in the peripheral nervous system unique interactions of unique regenerative genes with unique neuronal enhancers are formed.
‘Our work has many uses throughout neuronal biology and provides new directions for fresh repair approaches,’ Palmisano added. Future directions will be to know how the cohesin protein is activated following a nerve injury. Subsequently, we are capable of enhancing, cohesin promoting regeneration in conditions that are weak or not existent, for example the central nervous system.
Reference:
State O. Mouse study explores how nerve cells repair themselves.
