Jordi Guimera-Vilaro Edit Profile
In 1992 Jordi studied at the University of Barcelona in Barcelona, Catalonia, Spain at the faculty of Genetics. In two years he was a student of the St. Mary’s Hospital Medical School in London, United Kingdom. He studied at the faculty of Biochemistry and Molecular Genetics. In 1995 he studied at Queen's University of Belfast in Belfast, Northern Ireland. He received a degree of the Bachelor in English. From 1995 to 1996 he studied at the University of Texas Southwestern Medical Center in Dallas, Texas, United States. He studied at the Department of Molecular Genetics.
In 1996 he studied at the University of Murcia in Murcia, Spain at the faculty of anatomy. He graduated from it in 1997. In a year he was a student of the Institute of Mammalian Genetics in Munich, Germany. He became a Post-Doctorial. In this year he was a student of the University of Barcelona in Barcelona, Catalonia, Spain. he received a degree of the Doctor of Biology. From 2000 to 2001 he studied at Karolinska Institute and Stockholm University in Stockhol, Sweden at the faculty of Cell and Molecular Biology.
In 1992 Jordi started working in the human genetics field as a research assistant at the Biomedical Research Institute in Barcelona, Spain working on the construction of a linkage map integrated into the cytogenetic, genetic and YAC maps of human chromosome 21. At the end of 1993, he began his Ph.D. studies at the Department of Molecular Genetics at the Cancer Research Institute in Barcelona, Spain under the supervision of Professor Xavier Estivill, in isolating new genes involved in the mental retardation of Down syndrome. Human cosmid libraries were constructed and a YAC, cosmid contig was generated from the Down syndrome critical region (a region on the long arm of chromosome 21 thought to be responsible for most of the features of Down syndrome, including the severe intellectual disability). His further research carried out at the University of Texas, Southwestern Medical Center in Dallas, Texas, United States, and at the University of London, St Mary's Hospital Medical School in London, England. Prof. Bob Williamson was pivotal for the discovery of 37 novel human genes and the 1st generation of a transcriptional map covering the Down syndrome critical region. His studies culminated in the identification and characterization of the Minibrain gene (MNB-Dyrk1a) as a putative neurogenic factor that, when misexpressed, is involved in the intellectual disability observed in individuals with Down syndrome. Gain and loss-of-function studies in mouse models demonstrated that MNB is responsible for the learning deficits and other dysfunctions that may be associated with Down syndrome. Modern molecular genetic technics combined with morphological and developmental studies carried out at the University of Medicine (Murcia, Prof. Salvador Martínez and Prof. Luís Puelles) completed his scientific formation. In 1998 received his doctoral degrees in Biology (summa cum laude by unanimity) by the University of Barcelona.
As the recipient of a Marie Curie research fellowship from 1998 to 2000), Dr. Guimera continued his postdoctoral research in the developmental genetics field in the Institute of Mammalian Genetics at the GSF Center (Munich, Germany; Prof. Rudi Balling). He is currently Principal Investigator in the Institute of Development genetics at the Helmholtz Zentrum München. Much of his work in mouse genetics has focused on the development and function of midbrain GABAergic neurogenesis. His research group aimed to discover the genetics and the mechanisms underlying the dorsal, ventral midbrain GABAergic neurogenesis. His major scientific achievement at present is the identification and characterization of a novel bHLH gene (Megane) as a cell fate determinant of midbrain GABAergic neurogenesis, as determined by gene targeting-homologous recombination in mouse embryonic stem cells. He is currently generating new mouse models involving gain, and loss-of-function experiments to decipher the mechanisms underlying the specification of the GABAergic neurons in the brain and investigate their potential involvement in human diseases when misregulated. In addition, his group presented recently a novel conceptual advance regarding the two most important bHLH families involved in neurogenesis. Neurogenesis depends essentially on the balance between transcription factors belonging to the hairy, E(spl) and proneural families. These two families have long been believed to counterpart each other’s function. The conceptual advances provided by the findings presented in this study uncover the first synergistic cooperation between these two families provides a novel paradigm for how these two families cooperate for the acquisition of GABAergic neuronal identity, outlines the underlying mechanisms, and defines a new model for dorsal, ventral midbrain GABAergic neurogenesis.
The significance of these findings for the broader community is given by the fact that Gamma-aminobutyric acid (GABA) is the primary inhibitory neurotransmitter in the mature brain. Many neurological conditions such as schizophrenia, bipolar disorder, epilepsy, anxiety, Huntington’s disease, chronic pain, and addiction are associated with a remarkable dysfunctional GABAergic inhibition. Finding the factors dictating GABAergic neuronal specification and concomitantly understanding the molecular mechanisms and functional interactions between these factors is one of the major challenges in developmental neurogenesis and it is essential for cell therapy strategies in which the GABAergic system is disturbed.
Jordi married to Maria-Jose Cuevas-Alonso. Children: Felip, Nil, Anna.
1987 - 1992
1992 - 1993
1993 - 1998
1995 - 1996
1996 - 1997
2000 - 2001
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