Gerry Downes

Gerald "Gerry" Downes is an associate professor in biology at the University of Massachusetts, Amherst. His research expertise is in the genetic requirements for zebrafish swimming. Recently he has expanded his research interests into using the zebrafish system to model idiopathic (unknown cause) epilepsy syndromes.

Career history

Downes received his Bachelors in biology at Johnson C. Smith University in Charlotte, North Carolina, and his PhD in Neuroscience with Narasimhan Gautam at Washington University in St. Louis, Missouri. He then moved to Philadelphia and performed a postdoctoral fellowship with Michael Granato at the University of Pennsylvania between 1999 and 2005. He started as an Assistant Professor of biology at the University of Massachusetts Amherst in 2005, and was promoted to Associate Professor in 2012.

Research

During his postdoctoral fellowship Downes started to work with the zebrafish (Danio rerio) model system. Zebrafish make a great model organism for neuroscience research because they develop quickly and are transparent so their brains and brain development can be easily observed.[1] Furthermore, there are considerable similarity in the genes and pathways involved in brain development between humans and zebrafish.[2] As a postdoctoral fellow, Downes helped develop a method, stochastic labeling, to track the development of individual neurons in intact zebrafish using green fluorescent protein (GFP), which is essential for understanding how neurons grow directionally and form connections in the nervous system.[3] He also started to work on a class of zebrafish mutants that exhibit abnormal swimming behaviors that were isolated from a previous genetic screen.[4] When he started work on this project the identities of the underlying genes weren't known. However, his work showed that mutations in the neurotransmitter-degrading enzyme acetylcholinesterase cause abnormal swimming behavior in one line of mutant zebrafish.[5] In collaboration with John Kuwada's laboratory at the University of Michigan, they also discovered mutations in a zebrafish glycine receptor underlie abnormal swimming in another line of zebrafish[6]

At the University of Massachusetts, Downes continued his work on zebrafish mutants that exhibit abnormal swimming behavior. His group identified mutations in a muscle cell calcium pump critical for muscle relaxation,[7] a mitochondrial enzyme required to break down a subset of amino acids,[8] and a neurotransmitter transporter[9] from three different lines of zebrafish mutants. These zebrafish mutants parallel and serve as new animal models for Brody's Disease, a severe muscle weakness disorder; Maple Syrup Urine Disease, a metabolic disorder that can cause severe neurological damage,[10] and a generalized epilepsy disorder.

Downes is continuing to lead a team of researchers at the University of Massachusetts, who focus on determining the genes and neural networks involved in movement. Downes' laboratory is also working to better understand and developing new treatments for epilepsies.[11]

References
  1. Burke, Elizabeth (August 8, 2016). "Why Use Zebrafish to Study Human Diseases?". NIH Intramural Research Program. Retrieved September 19, 2020.
  2. Monesson-Olson, Bryan; McClain, Jon J.; Case, Abigail E.; Dorman, Hanna E.; Turkewitz, Daniel R.; Steiner, Aaron B.; Downes, Gerald B. (2018). "Expression of the eight GABAA receptor α subunits in the developing zebrafish central nervous system". PLOS ONE. 13 (4): e0196083. Bibcode:2018PLoSO..1396083M. doi:10.1371/journal.pone.0196083. ISSN 1932-6203. PMC 5922542. PMID 29702678.
  3. Downes, Gerald B.; Waterbury, Julie A.; Granato, Michael (November 2002). "Rapid in vivo labeling of identified zebrafish neurons". Genesis. 34 (3): 196–202. doi:10.1002/gene.10120. ISSN 1526-954X. PMID 12395384. S2CID 8656186.
  4. Nüsslein-Volhard, Christiane (November 2012). "The zebrafish issue of Development". Development (Cambridge, England). 139 (22): 4099–4103. doi:10.1242/dev.085217. ISSN 1477-9129. PMID 23093421. S2CID 7854819.
  5. Downes, Gerald B.; Granato, Michael (June 1, 2004). "Acetylcholinesterase function is dispensable for sensory neurite growth but is critical for neuromuscular synapse stability". Developmental Biology. 270 (1): 232–245. doi:10.1016/j.ydbio.2004.02.027. ISSN 0012-1606. PMID 15136152.
  6. Hirata, Hiromi; Saint-Amant, Louis; Downes, Gerald B.; Cui, Wilson W.; Zhou, Weibin; Granato, Michael; Kuwada, John Y. (June 7, 2005). "Zebrafish bandoneon mutants display behavioral defects due to a mutation in the glycine receptor beta-subunit". Proceedings of the National Academy of Sciences of the United States of America. 102 (23): 8345–8350. Bibcode:2005PNAS..102.8345H. doi:10.1073/pnas.0500862102. ISSN 0027-8424. PMC 1149420. PMID 15928085.
  7. Olson, Bryan D.; Sgourdou, Paraskevi; Downes, Gerald B. (June 2010). "Analysis of a zebrafish behavioral mutant reveals a dominant mutation in atp2a1/SERCA1". Genesis. 48 (6): 354–361. doi:10.1002/dvg.20631. ISSN 1526-968X. PMC 2885577. PMID 20533403.
  8. Friedrich, Timo; Lambert, Aaron M.; Masino, Mark A.; Downes, Gerald B. (March 2012). "Mutation of zebrafish dihydrolipoamide branched-chain transacylase E2 results in motor dysfunction and models maple syrup urine disease". Disease Models & Mechanisms. 5 (2): 248–258. doi:10.1242/dmm.008383. ISSN 1754-8411. PMC 3291646. PMID 22046030.
  9. McKeown, Kelly Anne; Moreno, Rosa; Hall, Victoria L.; Ribera, Angeles B.; Downes, Gerald B. (February 15, 2012). "Disruption of Eaat2b, a glutamate transporter, results in abnormal motor behaviors in developing zebrafish". Developmental Biology. 362 (2): 162–171. doi:10.1016/j.ydbio.2011.11.001. ISSN 1095-564X. PMC 4013685. PMID 22094018.
  10. Roberts, Nathan B. (July 2012). "Maple syrup urine disease: new insights from a zebrafish model". Disease Models & Mechanisms. 5 (4): 417–418. doi:10.1242/dmm.010272. ISSN 1754-8411. PMC 3380704. PMID 22730471.
  11. "Research". Downes Laboratory. UMass Amherst.
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