Project Summary:

With an interest in examining how altered cytologic architecture and connectivity result in disease, I have begun work on the genetic model of Fragile X Syndrome (FraX) in Drosophlia.  FraX is caused by the loss of function in a single gene, FMR1, and is the most commonly inherited form of mental retardation and autism spectrum disorders.  At the molecular level, this is mediated by a trinucleotide repeat expansion in the gene that precludes its protein expression and results in altered translational regulation of down stream targets. 

I am most interested in exploring the morphologic and underpinning cytoskeletal dynamics associated with, and perhaps causing, the impairments in this disease model. First, it is critical to determine the period of requirement for FMRP function in the nervous system.  Is FraX a ‘disease of development’ indicating a transient requirement for FMRP or a ‘disease of plasticity’ indicating a maintained, constitutive requirement for FMRP? Astoundingly, this fundamental question has not been sufficiently addressed. Using genetic techniques (Geneswitch System) to determine the temporal requirements of FMRP in the Drosophila model, our readouts will include molecular changes in synaptic proteins, neuronal architecture, and behavior. Second, I will test the hypothesis that FMRP plays a primary role in the regulation of the neuronal cytoskeleton. I will examine the cytoskeleton directly, primarily in neuronal cultures, for changes in growth dynamics and structure. I will be particularly interested in examining the cytoskeleton during growth cone behavior and subsequent synaptogenesis.

 

Education:

INSTITUTION AND LOCATION	DEGREE	YEAR(s)	FIELD OF STUDY
College of the Holy Cross, Worcester, MA	B.A.	1994-1998	Biology
University of Massachusetts Graduate School of	Ph.D.	1998-2004	Cell Biology
Biomedical Science, Worcester, MA
Children’s Hospital, Harvard Medical, Boston, MA	Postdoctoral	2004-2005	Neuroscience
Vanderbilt University, Nashville, TN	Postdoctoral	2006-present	Neuroscience

 

Publications:

Luna E.J., K.N. Pestonjamasp, T. Nebl, Y. Chen, C. Gatto, S.W. Oh, and R.K. Pope. 2001. “Motile Membrane Skeletons: What Neutrophils and Muscle Have in Common.” Cell Mol Biol 6(2): 219.

Ledbetter M.L.S. and C.L. Gatto. 2003. “Concentrations of ouabain that prevent intercellular communication do not affect free calcium levels in cultured fibroblasts.” Cellular Biochemistry and Function 21: 363-370.

Chen, Y., N. Takizawa, J. Crowley, S.W. Oh, C.L. Gatto, T. Kambara, O. Sato, M. Ikebe, and E.J. Luna. 2003. “F-Actin and Myosin II Binding Domains in Supervillin.” J Biol Chem 278(46): 46094-46106.

Gatto C.L., B.J. Walker, and S. Lambert. 2003.  “Local ERM activation and dynamic growth cones at Schwann cell tips implicated in efficient Node of Ranvier Formation.” J Cell Biol 162(3): 489-498.

Gatto, C.L., B.J. Walker, and S. Lambert.  2007. “Asymmetric ERM activation is required for directed process retraction, migration, and maintenance of polarity in mature Schwann cells.” J. Cell. Physiol. 210: 122-132.

 

Professional membership:

1998-present American Society for Cell Biology

 

Cultured Primary Drosophila Neurons
Prepared from pupae at 5 hours post head eversion – shown at 3 days in vitro
Green: UAS-GFP driven by GAL4-OK107 showing Mushroom Body Kenyon Cells
Red: synapsin
Blue: HRP