Prof. Nigel Atkinson
Office: PAT 228
phone: (512) 232-3404
email:
Nigel Atkinson received his Ph.D. in Biochemistry from the M.S. Hershey Medical School in 1986 and conducted his postdoctoral studies from 1986-1991 in Genetics and Neurobiology at the University of Wisconsin at Madison. He joined the faculty at the University of Texas in 1991. He has served on several NIH Review Panels and is an Assistant Editor for Biochemical Genetics. Dr. Atkinson was a Dean’s Fellow for Research in 2001 and also received a College of Natural Sciences Teaching Excellence Award that year. He currently is Associate Professor of Neurobiology at the University of Texas.
Research Interests
Ion channels produce the electrical impulses that the nervous system uses to transmit information. Each neuron can produce a large number of different channels. The channels that it chooses to express determine its electrical properties and ultimately the electrical character of the nervous system itself.
The fundamental question that drives us is: How are ion channel genes regulated and what are the consequences of this regulation? To address this question we have been using the slowpoke gene of Drosophila as a model. The slowpoke gene encodes the BK-type Ca2+-activated K+ channel. This ion channel is not opened by voltage or by a chemical, but rather is opened when intracellular calcium levels rise. Calcium then binds to the channel causing it to open. The channels is permeable to K+, and causes an inhibitory response due to the hyperpolarization of the membrane potential. In insects and mammals these channels are used in both nervous tissue and muscle. In humans this channel plays a central role in controlling blood pressure.
We have shown that the complex pattern of slowpoke expression is produced by a complex transcriptional control region. With the use of transgenes we identified multiple tissue-specific promoters and novel control elements that stimulate expression in specific tissues and even specific muscle subsets. We are now focused on identifying the DNA control elements that specify neural subtype-specific expression. An unusual aspect of our work is that we have correlated changes in expression pattern with changes in cellular electrophysiological properties and behavioral changes in the animal. We have begun to analyze other K+ channel genes in the hopes of detecting common regulatory themes.
Recently, we have started a new initiative to understand the role this Ca2+-activated K+ channel might play in the acute side-effects of exposure to organic solvent inhalants and to alcohol. The inhalants, which are abused by a startling large number of adolescents, are components of many common household cleaning solutions and fuels. We have observed that after Drosophila recover from being knocked out by benzyl alcohol vapor or ethanol they exhibit resistance upon re-exposure. Concomitant with recovery we have observed that mRNA from the slowpoke Ca2+-activated K+ channel gene increases in abundance. Using transgenic flies we have shown that this occurs because of changes in the regulation of the slowpoke gene. If slowpoke is involved in the appearance of resistance then artificially manipulating the level of slowpoke expression should alter resistance. Using transgenes and mutants we have artificially manipulated slowpoke expression. These animals have changed recovery rates from solvent anesthesia. In the future we hope to identify the transcriptional regulatory pathways that produce this effect using both molecular and classical genetic tools.