Ian Mattaj, came to the PRBB last October for the celebration of the 10th anniversary of the CRG. This Scottish researcher is the director of the European Molecular Biology Laboratory (EMBL) in Heidelberg, the largest molecular biology institution in Europe. He is also president of the CRG’s scientific advisory board, and he gave us his view on science at the CRG, in Catalonia, Spain and Europe.
How would you sum up the CRG´s first 10 years?
The CRG is remarkably successful for such a young institution. They have been recruiting foreign researchers, not so common in Spain, and they have set up some excellent programmes. It usually takes about 10 to 15 years for a research centre to really develop high quality, but the CRG has done so from the beginning. They have put in place mechanisms, some of them copied from the EMBL, which help ensure the quality of the research.
How has being part of the PRBB helped?
The CRG has no critical mass in every area, so having colleagues close by has definitely helped. We have just done the evaluations of the groups and I have heard about research clubs for neuroscience and computational biology, where researchers from the various centres at the PRBB, and even from other groups in Barcelona, meet and discuss their work every two weeks. This type of environment is really advantageous; it helps foster good research.
What do you think of current research in Catalonia and Spain?
Spain has produced many brilliant scientists, so the education system is obviously working, but the organisation of the public research system and researchers needs to change, along the lines we see in some institutes such as the CRG. Also continuous strong support from the political area is needed. The message of the Catalan government has been to support research that is excellent at international standard, and this is obviously the right way to improve all scientific productivity and even help the country.
How is the economic crisis affecting the R&D system in Europe?
Different countries have different degrees of economic problems, and some like Sweden or Germany have actually increased their budget for science, because they believe it is a good weapon to help fight possible future crises. In other countries I understand that cuts might be needed, but there are different ways to make them. In my opinion, if necessary, only non-high quality research should be cut.
What are the biggest challenges in molecular biology for the coming years?
There are different sorts of challenges. There are aspects of biology about which we know so little that we cannot even imagine understanding them, such as how the brain works to produce consciousness, the sense of self etc., that it is a big long-term challenge.
In the shorter term, I think an important issue will be how we can apply the recent technological developments in biomedicine, such as next generation sequencing, to improve our health. The possibilities are endless, but so far they are only possibilities.
Several studies have suggested that daily caffeine administration can protect against brain injury in some cases, for example in animal models of neurodegenerative diseases, such as Parkinson’s and Alzheimer’s diseases, as well as in ischemic and traumatic brain injury, or allergic encephalitis. Olga Valverde’s group at the CEXS-UPF decided to check if it could also have a positive effect on MDMA-induced neuroinflammation.
The recreational drug MDMA, or ecstasy, induces astrocytic and microglial activation in mice striatum, which leads to inflammation and neurotoxicity. They injected caffeine (10, 20, or 30 mg/kg, i.p) for 21 consecutive days into mice, and then on day 22, mice pretreated with caffeine or saline (controls) received a neurotoxic regimen of MDMA (3 × 20 mg/kg, i.p., 2-h interval) or saline. Changes in body temperature were evaluated. Forty-eight hours after the last MDMA or saline injection, behavioral parameters such as locomotor activity, sensorimotor reflexes, and anxiety were investigated and microglia and astroglia activation to MDMA treatment was examined in the mouse striatum.
The results, published in the journal Psychopharmacology, show that consuming regularly low doses of caffeine (10 mg/kg) completely prevented MDMA-induced glial activation without inducing physiological or behavioral alterations in any of the assays performed. Therefore, caffeine can have anti-inflammatory effects on ecstasy-induced neuroinflammation in mice.
Ruiz-Medina J, Pinto-Xavier A, Rodríguez-Arias M, Miñarro J, Valverde O. Influence of chronic caffeine on MDMA-induced behavioral and neuroinflammatory response in mice. Psychopharmacology (Berl). 2012 Nov 29;
The “8th European Zebrafish Meeting” will be held at the Palau de Congressos de Catalunya, 9-13 July 2013. Organisers include Berta Alsina, from the CEXS-UPF, as well as Angela Nieto (CSIC-Alicante), Paola Bovolenta (CSIC-Madrid), Jose Luis Gómez-Skarmeta (CSIC-Sevilla), Enrique Martin Blanco (CSIC,Barcelona) and Miguel Angel Pardo (Azti-Tecnalia, Derio).
The meeting is intended to serve as a platform of communication for researchers working in zebrafish, a community that has expanded exponentially over the last decade. The European biannual meeting.
Among many others, topics will cover new advances in life imaging, patterning, disease models, gene regulation and genomics, circuits and behaviour, drug screening and cancer.
Prof Sydney Brenner and Prof Denis Duboule, as keynote speakers working with other model organisms, will highlight their discoveries in C.elegans and mouse genetics.
For more information, please see http://www.zebrafish2013.org.
Remember to register early!
Deadline Abstract Submission: 24 March 2013
Deadline Early Registration: 30 May 2013
Cancer is generally caused by a combination of many specific mutations, called drivers. But cancer cells contain many other mutations that are not the cause of the cancer, but rather a consequence (passenger mutations). Also, high-throughput genome projects are identifying a huge number of somatic variants. Which ones are cancer-causing? How to distinguish the needle in the haystack?
A new computational method recently published in Genome Medicine by the research group led by Núria López-Bigas at the GRIB (UPF-IMIM), can help. Called transformed Functional Impact Score for Cancer (transFIC), it improves the assessment of the functional impact of tumor nonsynonymous single nucleotide variants (nsSNVs) by taking into account the baseline tolerance of genes to functional variants.
Other methods predicting the functional impact of cancer-causing somatic variants employ evolutionary information to assess the likely impact of an amino acid change on the structure or function of the altered protein. However, according to the authors, the ultimate effect of this amino acid change on the functioning of a cell depends on other factors as well, such as the particular role played by the altered protein in the cellular machinery. The more critical that role is, the less tolerant will the protein be to an amino acid change.
Their new method takes this feature into consideration, and has been shown to outperform previous ones. They distribute their new tool as a PERL script that users can download and use locally, and they have set up a web server which can be queried to obtain the transFIC of somatic cancer nsSNVs.
Gonzalez-Perez A, Deu-Pons J, Lopez-Bigas N. Improving the prediction of the functional impact of cancer mutations by baseline tolerance transformation. Genome Med. 2012 Nov 26;4(11):89