Eric H Lyons

Eric H Lyons

Associate Professor, Plant Science
Associate Professor, Agricultural-Biosystems Engineering
Advisor, CALS' Office of the Assoc Dean - Research for Cyber Initiatives in Agricultural / Life - Vet Science
Associate Professor, Genetics - GIDP
Associate Professor, BIO5 Institute
Primary Department
Department Affiliations
Contact
(520) 626-5070

Research Interest

Eric Lyons, PhD is an assistant professor at the University of Arizona School of Plant Sciences. Dr. Lyons is internationally known for his work in understanding the evolution, structure, and dynamics of genomes. Core to his research activities is the development of software systems for managing and analyzing genomic data and cyberinfrastructure for the life sciences.Dr. Lyons has published over 30 original research papers and 5 book chapters, many in collaboration with investigators from around the world. He is a frequent presenter at national and international meetings, and has been invited to teach workshops on the analysis of genomic data to plant, vertebrate, invertebrate, microbe, and health researchers.Prior to joining the faculty in the School of Plant Sciences, Dr. Lyons worked with the iPlant Collaborative developing cyberinfrastructure, and managing its scientific activities. In addition, he spent five years working in industry at biotech, pharmaceutical, and software companies. Dr. Lyons’ core software system for managing and analyzing genomic data is called CoGe, and is available for use at http://genomevolution.org

Publications

Foley, S. W., Gosai, S. J., Wang, D., Selamoglu, N., Sollitti, A. C., K\"oster, T., Steffen, A., Lyons, E., Daldal, F., Garcia, B. A., & others, . (2017). A global view of RNA-protein interactions identifies post-transcriptional regulators of root hair cell fate. Developmental cell, 41(2), 204--220.
Thomas, B. C., Rapaka, L., Lyons, E., Pedersen, B., & Freeling, M. (2007). Arabidopsis intragenomic conserved noncoding sequence. Proceedings of the National Academy of Sciences of the United States of America, 104(9), 3348-3353.

PMID: 17301222;PMCID: PMC1805546;Abstract:

After the most recent tetraploidy in the Arabidopsis lineage, most gene pairs lost one, but not both, of their duplicates. We manually inspected the 3,179 retained gene pairs and their surrounding gene space still present in the genome using a custom-made viewer application. The display of these pairs allowed us to define intragenic conserved noncoding sequences (CNSs), identify exon annotation errors, and discover potentially new genes. Using a strict algorithm to sort high-scoring pair sequences from the bl2seq data, we created a database of 14,944 intragenomic Arabidopsis CNSs. The mean CNS length is 31 bp, ranging from 15 to 285 bp. There are ≈1.7 CNSs associated with a typical gene, and Arabidopsis CNSs are found in all areas around exons, most frequently in the 5′ upstream region. Gene ontology classifications related to transcription, regulation, or "response to..." external or endogenous stimuli, especially hormones, tend to be significantly overrepresented among genes containing a large number of CNSs, whereas protein localization, transport, and metabolism are common among genes with no CNSs. There is a 1.5% overlap between these CNSs and the 218,982 putative RNAs in the Arabidopsis Small RNA Project database, allowing for two mismatches. These CNSs provide a unique set of noncoding sequences enriched for function. CMS function is implied by evolutionary conservation and independently supported because CNS-richness predicts regulatory gene ontology categories. © 2007 by The National Academy of Sciences of the USA.

VanBuren, R., Bryant, D., Bushakra, J. M., Vining, K. J., Edger, P. P., Rowley, E. R., Priest, H. D., Michael, T. P., Lyons, E., Filichkin, S. A., & others, . (2016). The genome of black raspberry (Rubus occidentalis). The Plant Journal, 87(6), 535--547.
Lyons, E., Pedersen, B., Kane, J., Alam, M., Ming, R., Tang, H., Wang, X., Bowers, J., Paterson, A., Lisch, D., & Freeling, M. (2008). Finding and comparing syntenic regions among Arabidopsis and the outgroups papaya, poplar, and grape: CoGe with rosids. Plant Physiology, 148(4), 1772-1781.

PMID: 18952863;PMCID: PMC2593677;Abstract:

In addition to the genomes of Arabidopsis (Arabidopsis thaliana) and poplar (Populus trichocarpa), two near-complete rosid genome sequences, grape (Vitis vinifera) and papaya (Carica papaya), have been recently released. The phylogenetic relationship among these four genomes and the placement of their three independent, fractionated tetraploidies sum to a powerful comparative genomic system. CoGe, a platform of multiple whole or near-complete genome sequences, provides an integrative Web-based system to find and align syntenic chromosomal regions and visualize the output in an intuitive and interactive manner. CoGe has been customized to specifically support comparisons among the rosids. Crucial facts and definitions are presented to clearly describe the sorts of biological questions that might be answered in part using CoGe, including patterns of DNA conservation, accuracy of annotation, transposability of individual genes, subfunctionalization and/or fractionation of syntenic gene sets, and conserved noncoding sequence content. This précis of an online tutorial, CoGe with Rosids (http://tinyurl.com/4a23pk), presents sample results graphically. © 2008 American Society of Plant Biologists.

Holbrook, S., Finley, J. K., Lyons, E. L., & Herman, T. G. (2012). Loss of syd-1 from R7 neurons disrupts two distinct phases of presynaptic development. The Journal of neuroscience : the official journal of the Society for Neuroscience, 32(50), 18101-11.

Genetic analyses in both worm and fly have identified the RhoGAP-like protein Syd-1 as a key positive regulator of presynaptic assembly. In worm, loss of syd-1 can be fully rescued by overexpressing wild-type Liprin-α, suggesting that the primary function of Syd-1 in this process is to recruit Liprin-α. We show that loss of syd-1 from Drosophila R7 photoreceptors causes two morphological defects that occur at distinct developmental time points. First, syd-1 mutant R7 axons often fail to form terminal boutons in their normal M6 target layer. Later, those mutant axons that do contact M6 often project thin extensions beyond it. We find that the earlier defect coincides with a failure to localize synaptic vesicles, suggesting that it reflects a failure in presynaptic assembly. We then analyze the relationship between syd-1 and Liprin-α in R7s. We find that loss of Liprin-α causes a stronger early R7 defect and provide a possible explanation for this disparity: we show that Liprin-α promotes Kinesin-3/Unc-104/Imac-mediated axon transport independently of Syd-1 and that Kinesin-3/Unc-104/Imac is required for normal R7 bouton formation. Unlike loss of syd-1, loss of Liprin-α does not cause late R7 extensions. We show that overexpressing Liprin-α partly rescues the early but not the late syd-1 mutant R7 defect. We therefore conclude that the two defects are caused by distinct molecular mechanisms. We find that Trio overexpression rescues both syd-1 defects and that trio and syd-1 have similar loss- and gain-of-function phenotypes, suggesting that the primary function of Syd-1 in R7s may be to promote Trio activity.