The Excellent Paper in Neuroscience Award
ERA-Net Neuron announced the winner of the second year of the “Excellent Paper in Neuroscience Award“ (EPNA) for young scientists for the year 2010. The award was given in a ceremony during the European Neurodegenerative Diseases-2011 meeting on ‘Biology to Drugs & Therapeutics’ in Rome on October 10th, 2011.
In June 2010, ERA-Net NEURON had published the second call for applications for the “Excellent Paper in Neuroscience Award”. The winner and awardee for 2010 was Dr. Jens Schwamborn from the Westfalian Wilhelms-University Muenster, Institute of Cell Biology, Stem Cell Biology and Regeneration, Germany.
|During the European Neurodegenerative Diseases-2011 meeting on
Biology to Drugs & Therapeutics, the ceremony for the Award 2010 took place.
|From left to right: Dr. Jens Schwamborn, Dr. Erkki Raulo, within NEURON responsible for the
management of the award and PD Dr. M. Dorlöchter, the coordinator of the ERA-NET NEURON.
As in the year before the ceremony took place within a scientific meeting on ‘Biology to Drugs & Therapeutics’ that was held near Rome in October 2011. “This offers a perfect opportunity to the young scientist to present his work in a regular talk for an international audience and thus gives them high visibility”, as Dr. Raulo pointed out in his introductory note.
Dr. Schwamborn presented thus his results in an ERA-NET NEURON Young Scientist Lecture with the title: ”Differentiation and stemness maintenance of neural stem cells”
He received the award on his publication in Cell (2009) describing that the subcellular localization of TRIM32 in neural stem cells regulates the balance between stemness maintenance and differentiation. Neural stem cells express the differentiation inducing factor TRIM32 long before undergoing neuronal differentiation. Why are they then able to maintain their stemness although they express TRIM32? In other words, which molecular mechanisms ensure the maintenance of stemness characteristics in neural stem cells over several rounds of cell divisions? The paper with new data to answer these questions was entitled: ‘The TRIM-NHL protein TRIM32 activates microRNAs and prevents self-renewal in mouse neural progenitors’ (Cell 136, 913-25).
For the coordinator of the ERA-NET NEURON, Dr. Marlies Dorlöchter, ”The Excellent Paper in Neuroscience Award was established in NEURON as an instrument of support for outstanding young researchers in neuroscience. The award is a central part of NEURON visibility towards young research community in the ERA-NET NEURON partner countries increasing attractiveness of devoted researcher’s career. Dr. Schwamborn has made significant contributions towards our understanding of disease and injury of the nervous system.”
Dr. Schwamborn’s summary of the presentation at the European Neurodegenerative Diseases-2011 meeting on ‘Biology to Drugs & Therapeutics’
In the mouse neocortex during development, neural stem cells produce all the neurons of the Cortex. A defining feature of these stem cells is their ability to undergo asymmetric divisions, thereby giving rise to one new daughter stem cell and one cell that differentiates into a neuron. This maintenance of self-renewal capacities is of critical importance for brain development. However, so far the mechanisms that balance self-renewal and neuronal differentiation are rather unknown.
We have been showing that the TRIM-NHL protein TRIM32 regulates protein degradation and microRNA activity to control the balance between those two daughter cell types. In both horizontally and vertically dividing progenitors, TRIM32 becomes polarized in mitosis and is concentrated in one of the two daughter cells. TRIM32 overex-pression induces neuronal differentiation while inhibition of TRIM32 causes both daughter cells to retain progenitor cell fate. TRIM32 ubiquitinates and degrades the transcription factor c-Myc but also binds Argonaute-1 and thereby increases the activity of specific microRNAs. We have shown that Let-7 is one of the TRIM32 targets and is required and sufficient for neuronal differentiation.
Interestingly, neural stem cells express the differentiation inducing factor TRIM32 long before they undergo neuronal differentiation. The reason why neural stem cells are able to maintain their stemness although they express TRIM32 has not been determined so far. In other words, which molecular mechanisms ensure the maintenance of stemness characteristics in neural stem cells over several rounds of cell divisions? Here we present some new data showing that the subcellular localization of TRIM32 in neural stem cells, regulates the balance between stemness maintenance and differentiation.