Skip to content. | Skip to navigation

Personal tools

Carme Gallego: Control of local mRNA expression

Lab Presentation

The connections in our brains are constantly changing. As we interact with our environment and with each other, the connections between our neurons are remodeled so that we can retain these interactions as learning and memory. At a molecular level, the brain accomplishes this remodeling in part by making new proteins at the specific sites where our neurons interact with each other (known as synapses). The process of synaptic remodeling, of strengthening and weakening of connections between neurons, is known as synaptic plasticity. Defects in synaptic plasticity are seen in many neurological disorders such as schizophrenia, fragile X mental retardation or spinal muscular atrophy. Our long-standing goal is the identification of molecular components of neuronal signalling cascades and determination of their role in synaptic plasticity.

Research Lines

Molecular mechanisms of neuronal plasticity: the role of KIS kinase
KIS is a protein kinase that associates with stathmin, a modulator of the tubulin cytoskeleton. KIS is found in RNA granules and stimulates translation of AMPA receptor subunits and PSD-95. Furthermore, KIS enhances β-actin polymerization in dendritic spines accordingly the absence of KIS produces morphological defects in synaptic spines. All these data suggest that KIS is a particularly attractive protein for the study of dendritic plasticity. Search for the synaptic inputs that activate KIS and identify endogenous targets will allow us to better understand the molecular mechanisms of synaptic plasticity
Synaptic plasticity and neurological disorders: the brain elongation factor eEF1A2 isoform
Synthesis of many synaptic proteins is under local control, and recent evidence suggests that modulation of the elongation steps of translation may be the key regulatory process underlying synaptic plasticity. Notably, the essential elongation factor eEF1A that binds the aminoacyl-tRNA to drive the first steps of translation elongation displays two very similar forms in vertebrates, eEF1A1 and eEF1A2. While the first is expressed throughout life in almost all tissues, the second form is specific to brain and skeletal muscle, pointing to specific roles of eEF1A2 in tissues where cellular plasticity is most relevant. The recent discovery that missense de novo mutations in eEF1A2 have causal effects in autism and epilepsy underline the relevance of this elongation factor in cognitive functions.
Functional relevance of intron retention mechanism in dendrites
We are interested in investigating the possibility of local splicing in synapses and the underlying molecular mechanisms. Published data and our own results show dendritic localization of several spliceosome related proteins. We hypothesize that dendritic splicing could be an important mechanism for increasing the molecular complexity and functional capacity of the synapse
Carme Gallego González
  • Carme Gallego
  • IBMB-CSIC
  • Baldiri Reixac, 15
  • 08028 Barcelona, Spain
  • Phone: +34 93 4020858 / +34 93 4020857
  • E-mail: cggbmc@ibmb.csic.es

Principal Investigator



Past students


Publications in the past 10 years:

  • GEORGIEVA MV, YAHYA G, CODÓ L, ORTÍZ R, TEIXIDÓ L, CLAROS J, JARA R, JARA M, IBORRA A, GELPÍ JL, GALLEGO C*, OROZCO M* & ALDEA M* (*corresponding authors) “Inntags: small self-structured epitopes aimed at innocuous protein tagging” Nature Methods 2015 12(10):955-8.

  • PEDRAZA N, ORTIZ R, CORNADÓ A, LLOBET A, ALDEA M & GALLEGO C “KIS, a kinase associated with microtubule regulators, enhances translation of AMPA receptors and stimulates dendritic spine remodeling” J Neurosci 2014, 34(42):13988-97.
     
  • YAHYA G,PARISI E, FLORES A, GALLEGO C & ALDEA M “A Whi7-Anchored Loop Controls the G1 Cdk-Cyclin Complex at Start” Mol Cell 2014, 53(1):115–126. 
     
  • FERREZUELO F, COLOMINA N, PALMISANO A, GARI E, GALLEGO C, CSIKASZ-NAGY A & ALDEA M “Critical size is set at a single-cell level by growth rate to attain homeostasis and adaptation” Nature Communications 2012, 3:1012doi:10.1038/ncomms  
     
  • ASENSIO-JUAN E; GALLEGO C & MARTÍNEZ-BALBÁS M “The histone demethylase PHF8 is essential for cytoskeleton dynamics” Nucleic Acids Research 2012 ;4Oct0(1429):99-40
     
  • BABA M,KELLER JR, SUN H-W, RESCH W, KUCHEN S, SUH HC, HASUMI H, HASUMI Y, KIEFFER-KWON K-R, GALLEGO C, HUGHES RM, KLEIN ME, OH HF, BIBLE P, SOUTHON E, TESSAROLLO L, SCHMIDT LS, LINEHAN WM,& CASELLAS R. “The Folliculin-Fnip1 pathway deleted in human Birt-Hogg-Dubé syndrome is required for B cell development” Blood 2012, 120(6):1254-61   
     
  • RUIZ-MIRÓ M, COLOMINA N, FERNÁNDEZ R, GARÍ E, GALLEGO C* & ALDEA M* (*corresponding authors)“Translokin interacts with cyclin D1 and prevents its nuclear accumulation during cellular quiescence” Traffic 2011 12(5):549-62.
     
  • PEDRAZA N, RAFEL M, NAVARROI, ENCINAS M, ALDEA M & GALLEGO C “Mixed-Lineage Kinase 2 phosphorylates transcription factor E47 and inhibits TrkB expression to link neuronal death and survival pathways”J. Biol. Chem 2009 284(47): 32980-8.  
     
  • CAMBRAY S, PEDRAZA N, RAFEL M, GARÍ E, ALDEA M & GALLEGO C “Protein kinase KIS localizes to RNA granules and enhances local translation” Mol. Cell. Biol. 2009, 29(3): 726-735. 
     
  • CARDUS A, PANIZO S, ENCINAS M, DOLCET X, GALLEGO C, ALDEA M, FERNANDEZ E & VALDIVIELSO JM “1,25-Dihydroxyvitamin D(3) regulates VEGF production through a vitamin D response element in the VEGFpromoter” Atherosclerosis. 2008, 204 (1):85-9.
     
  •  VERGES E, COLOMINA N, GARÍ E, GALLEGO C & ALDEA M “Cyclin Cln3 is retained at the ER and released by the J-chaperone Ydj1 in late G1 to trigger cell cycle entry” Mol Cell  2007, 26(5): 649–662.           
                                                                                    
  • CARDUS A, PARISI E, GALLEGO C, ALDEA M, FERNANDEZ E. & VALDIVIELSO JM“1,25-Dihydroxyvitamin D3 stimulates vascular smooth muscle cell proliferation through a VEGF-mediated pathway” Kidney Int. 2006, Apr;69(8):1377-84.  
     

Synaptic plasticity and neurological disorders: the brain elongation factor eEF1A2 isoform. 

  • AGENCY: MINECO BFU2014-52591-R
  • PERIOD: 2015-2017
  • PI: Carme Gallego. 

Molecular mechanisms of neuronal plasticity: the role of KIS kinase. 

  • AGENCY: MICINN BFU2011-25914
  • PERIOD: 2012-2014
  • PI: Carme Gallego. 
     

Plasticity and neuronal differentiation: regulation by KIS and MLK2 kinases.

  • AGENCY: MICINN BFU2008-01736/BFI
  • PERIOD: 2008 - 2011 
  • PI: Carme Gallego. 
     

Proliferation and neuronal differentiation: opposing effects of FGF and BDNF.

  • AGENCY: MEC, SAF2004-03142
  • PERIOD: 2005 - 2008
  • PI: Carme Gallego.
     

If you are interested in joining the lab as postdoc or PhD student please send us your CV and cover letter: Carme Gallego cggbmc@ibmb.csic.es

Document Actions