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Julia Dallman
Assistant Professor |
232 Cox Science Center, Dept. of Biology
1301 Memorial Drive, Coral Gables, FL 33124 |
(305) 284-3512
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| Education and Professional Experience |
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- 1987-1991, BA from the Dept. of Biology, Swarthmore College, Swarthmore PA
- 1991-1998, PhD from the Dept. of Zoology, University of Washington, Seattle WA Mentor: Dr. William J Moody
- 1998-2003, Post Doctoral Fellow, Dept. of Neurobiology, SUNY Stony Brook, NY Mentor: Dr. Gail Mandel
- 2003-2007, Research Assistant Professor, Dept. of Neurobiology, SUNY Stony Brook NY Mentor: Dr. Paul Brehm
- 2005, Co-lecturer-Comparative Invertebrate Embryology (Zool. 536) Friday Harbor Laboratories, University of Washington
- 2007, Assistant Professor, The University of Miami, Department of Biology
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| Awards |
- 1996, Society for Integrative & Comparative Biology-Best Student Paper Award
- 1995, Ingrith Deyrup-Olsen Award for Excellence in Teaching
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| Grants |
- 2004-2008, Principal Investigator NIH K01 Career Development Award Annual direct costs: $108,640
- 1998-2000, NIH Individual National Research Service Award
- 1995-1997, NSF Mathematical Biology Training Grant
- 1991-1994, NIH Molecular and Cellular Biology Training Grant
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| Areas of Focus |
| Development and Neuroscience |
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| Research Interests |
| My research focuses on understanding the genetic basis of swimming by studying a set of zebrafish mutants recently isolated in the lab. Zebrafish exhibit many similarities to humans in the genes and circuits that underlie movement. Therefore, zebrafish motility mutants provide useful models for human genetic diseases that impact nerve and muscle function. The lab also studies mutants for which the culprit gene has been identified, to better understand homeostatic mechanisms triggered in response to the mutation. The zebrafish motility mutant shocked has a point mutation in the glial glycine transporter (GlyT1). Consequently, the inhibitory neurotransmitter glycine builds up in the nervous system and the mutant larvae fail to escape when touched. However, as the larvae mature, they naturally recover the ability to mount a normal escape response. We have found that mutant recovery is associated with a dramatic decrease in the post-synaptic glycine receptors. We hope to further study this mutant with the aim of understanding the mechanisms causal to glycine receptor down-regulation. This study is medically relevant because glycine transporter antagonists are currently being tested as atypical anti-psychotics and similar forms of homeostasis are likely to occur in humans with chronic use of GlyT1 inhibitors. |
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| Teaching Interests |
| My goals in the classroom are not only to pass on information but also to convey my own excitement about the material as a means of encouraging students to think critically about the topics we cover. My aim is to make the students active participants in their learning. I also expose students to the primary literature and discuss the methods employed by the researchers so that the process by which we understand biological systems becomes apparent. |
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| Selected Publications |
- Dallman, JE, Walogorsky, MD, Brehm, P. Using high-speed camera and motion software to screen for zebrafish motility mutants. Manuscript in preparation.
- Mongeon, R, Gleason, MR, Masino, MA, Fetcho, JR, Mandel, G., and Brehm, P, Dallman JE. Synaptic homeostasis in a zebrafish glial glycine transporter mutant. Manuscript submitted to Neuron.
- Dallman JE, Gleason, M, Mongeon, R, Masino, M, Fetcho, J, and Brehm, P. The glycine transporter 1 is the gene mutated in the zebrafish motility mutant shocked. Program No. 749.11. 2005 Abstract Viewer and Itinerary Planner. Washington, DC: Society for Neuroscience, 2005. Online.
- Dallman JE, Allopenna, J, Bassett A, Travers A, Mandel G. (2004) A conserved role but different partners for the transcriptional corepressor CoREST in fly and mammalian nervous system formation. J Neurosci. 24(32):7186-93.
- Luna VM, Wang M, Ono F, Gleason MR, Dallman JE, Mandel G, Brehm P. (2004) Persistent electrical coupling and locomotory dysfunction in the zebrafish mutant shocked. J Neurophysiol. 92(4):2003-9.
- Gleason MR, Higashijima S, Dallman J, Liu K, Mandel G, Fetcho JR. (2003) Translocation of CaM kinase II to synaptic sites in vivo. Nat Neurosci.6(3):217-8.
- Dallman JE, Dorman JB, Moody WJ. (2000) Action potential waveform voltage clamp shows significance of different Ca2+ channel types in developing ascidian muscle. J Physiol. 524 Pt 2:375-86.
- Andres ME, Burger C, Peral-Rubio MJ, Battaglioli E, Anderson ME, Grimes J, Dallman J, Ballas N, Mandel G. (1999) CoREST: a functional corepressor required for regulation of neural-specific gene expression. Proc Natl Acad Sci U S A.96(17):9873-8.
- Dallman JE, Davis AK, Moody WJ. (1998) Spontaneous activity regulates calcium-dependent K+ current expression in developing ascidian muscle.J Physiol. 511 ( Pt 3):683-93. Featured article: see Perspectives in the same issue.
- Greaves AA, Davis AK, Dallman JE, Moody WJ. (1996) Co-ordinated modulation of Ca2+ and K+ currents during ascidian muscle development. J Physiol. 497 ( Pt 1):39-52.
- Davis AK, Greaves AA, Dallman JE, Moody WJ. (1995) Comparison of ionic currents expressed in immature and mature muscle cells of an ascidian larva. J Neurosci.15(7 Pt 1):4875-84.
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