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Contact
18111 Nordhoff Street
Northridge, CA 91330-8303
Phone: (818) 677-3356
Fax: (818) 677-2034
Email:biology.dept@csun.edu
Office Location:
Eucalyptus Hall 2102
Hours:
Mon-Fri: 8:00am-5:00pm
Maria Elena de Bellard
Assistant Professor
Ph.D., The City University of New York
email: mariaelenadotdebellardatcsundotedu
Phone: (818) 677-6470
Fax: (818) 677-2034
Office: Citrus Hall 3216B
Neural crest cells emerge from the neural tube early in development. They migrate extensively throughout the embryo and form most of the head and peripheral nervous system, giving rise to sensory and sympathetic ganglia, heart regions, glia, head bones, teeth, muscle cells, sensory organs, melanocytes and other cell types. The neural crest is interesting because of its unique origin, development and differentiation. These cells are initially part of the dorsal neural tube, with a clear epithelial character; later, they transform into actively motile mesenchymal cells. However, it remains unknown why neural crest cells target particular derivatives (neurons, heart muscle and glia) and body regions (peripheral nerves, heart, skin, head and gut).
The lab projects are:
1) Extend the study on the Slit2/Robo pathway on neural crest guidance.
Research carried in the past has shown how different adhesion and guidance molecules like ephrins, Sema3a and proteoglycans, play important roles in neural crest migration. In addition, we have recently shown that the axonal chemorepellants and branching factors Slits, expressed by non-migratory neural crest, also function as repellants for trunk, but not vagal neural crest cells and found interestingly, that Slits can enhance migration of trunk neural crest cells. These findings, plus the fact that Slits are expressed by the pre-migratory neural crest, suggest that these molecules play an important role in neural crest development.
2) Identify molecules that determine the specific migratory pathways decisions by neural crest cells.
We will make use of a technique developed during my postdoctoral studies that allows me to manipulate the migration of the neural crest in vitro and ex ovo during development. GDNF has been suggested to have such a chemoattractant role since enteric crest (neural crest cells that have migrated into the gut primordium) are attracted to GDNF and knockout mice for the neurotrophin and its receptors have severe deficits in the enteric nervous system.
3) Look at neural crest markers through evolution in sharks, snakes and lampreys.
The neural crest is responsible for the formation of the peripheral nervous system and head structures. We are looking into the evolution of neural crest in elasmobranches and other non-mammalian organisms by looking at the pattern of expression of genes like Sox10, Seraf, Sox2, etc during early development.
Publications:
de Bellard, ME and Bronner-Fraser, M. (2004). Neural crest migration methods in chicken embryo, in Cell migration in development, Jun-Lin Guan Ed., Humana Press series on Methods in Molecular Biology.
de Bellard, ME, Rao, Y. and Bronner-Fraser, M. (2003). Dual function of Slit2 in repulsion and enhanced migration of trunk neural crest cells. in press at J. Cell Bio, 162(2):269-279.
de Bellard, ME, Ching, W and Bronner-Fraser, M. (2002). Disruption of segmental neural crest migration and ephrin expression in Delta-1 null mice. Dev. Bio. 249:121-130.
Nellemann, C., de Bellard, ME, Barembaum, M, Laufer, E. and Bronner-Fraser, M. (2001) Excess lunatic fringe causes cranial neural crest over-proliferation. Dev Biol. 235(1):121-30. (First author also).
de Bellard, ME and Filbin, MT. (1999) Myelin-Associated Glycoprotein, MAG, binds specifically to a number of neuronal proteins. J. Neurosci. Res. 56(2):213-218.
Cai,D-M., Shen, Y-J., de Bellard, ME, Tang, S. and Filbin, M.T. (1999) Prior exposure to neurotrophins blocks inhibition of axonal regeneration by MAG and myelin via a cAMP-dependent mechanism. Neuron 22:89-101.
Shen, YJ de Bellard, ME, Salzer, J. L, Roder, J. and MT. Filbin (1998) Myelin-Associated glycoprotein (MAG) in myelin and expressed by Schwann cells inhibits axonal regeneration and branching. Molecular and Cellular Neuroscience 12:79-91. (First author also).
Tang, S., Woodhall, R., Shen, YJ, Saffel, J., de Bellard, ME, Doherty, P., Walsh, FS., and Filbin, MT. (1997) Soluble myelin-associated glycoprotein (MAG) found in vivo can inhibit axonal regeneration. Molecular and Cellular Neuroscience. 9:333-346.
Tang, S., Mukhopdhyay, G., Shen, Y-J, de Bellard, ME, Crocker, PR. and Filbin, MT. (1997) Myelin-associated glycoprotein (MAG) interacts with neurons via a sialic acid binding site at Arg118 and a distinct neurite inhibition site. J. Cell Biol. 138:1355-1366.
de Bellard, ME, S. Tang, G. Mukhopdadhyay, YJ Shen and MT. Filbin. (1996) Myelin-associated glycoprotein inhibits axonal regeneration from a variety of neurons via interaction with a sialoglycoprotein. Molecular and Cellular Neuroscience 7(2):89-101.
Filbin, MT., Mukhopadhyay, G., Tang, S., de Bellard, ME., Shen, YJ. (1996) Myelin-associated glycoprotein (MAG) as an inhibitor of axonal regeneration in both the PNS and the CNS. Peripheral nerve 7(1)1-14.