Parker B Antin
Associate Dean, Research-Agriculture and Life Sciences
Associate Vice President for Research, Agriculture - Life and Veterinary Sciences / Cooperative Extension
Professor, BIO5 Institute
Professor, Cellular and Molecular Medicine
Professor, Molecular and Cellular Biology
Primary Department
Department Affiliations
(520) 621-5242
Research Interest
Parker Antin is Professor of Cellular and Molecular Medicine in the College of Medicine, Associate Vice President for Research for the Division of Agriculture, Life and Veterinary Medicine, and Cooperative Extension, and Associate Dean for Research in the College of Agriculture and Life Sciences. In his positions of Associate Vice President and Associate Dean, he is responsible for developing and implementing the research vision for the Colleges of Agriculture and Life Sciences and the College of Veterinary Medicine, with total research expenditures of approximately $65M per year. His responsibilities include oversight of research strategy and portfolio investment, grants and contracts pre award services, research intensive faculty hires and retentions, research communication and marketing, research facilities, and research compliance services. In collaboration with Division and College leadership teams, he has shared responsibilities for philanthropy, budgets and information technology. Dr. Antin is a vertebrate developmental biologist whose research is concerned with the molecular mechanisms of embryonic development. His research has been supported by NIH, NSF, NASA, USDA, and the DOE, as well as several private foundations including the American Heart Association and the Muscular Dystrophy Association, He is the Principal Investigator of CyVerse, a $115M NSF funded cyberinfrastructure project whose mission is to design, deploy and expand a national cyberinfrastructure for life sciences research, and train scientists in its use (http://cyverse.org). With 65,000 users worldwide, CyVerse enables scientists to manage and store data and experiments, access high-performance computing, and share data and results with colleagues and the public. Dr. Antin is also active nationally in the areas of science policy and funding for science. He is a past President of the Federation of Societies for Experimental Biology (FASEB), an umbrella science policy and advocacy organization representing 32 scientific societies and 135,000 scientists. His continued work with FASEB, along with his duties as Associate Vice President and Associate Dean for Research, and CyVerse PI, brings him frequently to Washington, DC, where he advocates for support of science and science policy positions that enhance the scientific enterprise.

Publications

Darnell, D. K., Kaur, S., Stanislaw, S., Konieczka, J. H., Yatskievych, T. A., & Antin, P. B. (2007). Erratum: MicroRNA expression during chick embryo development (Developmental Dynamics 235 (3156-3165)). Developmental Dynamics, 236(1), 333-.
Kazmierski, S. T., Antin, P. B., Witt, C. C., Huebner, N., McElhinny, A. S., Labeit, S., & Gregorio, C. C. (2003). The complete mouse nebulin gene sequence and the identification of cardiac nebulin. Journal of Molecular Biology, 328(4), 835-846.
BIO5 Collaborators
Parker B Antin, Carol C Gregorio

PMID: 12729758;Abstract:

Nebulin is a giant (Mr 750-850kDa), modular sarcomeric protein proposed to regulate the assembly, and to specify the precise lengths of actin (thin) filaments in vertebrate skeletal muscles. Nebulin's potential role as a molecular template is based on its structural and biochemical properties. Its central ∼700kDa portion associates with actin along the entire length of the thin filament, its N-terminal region extends to thin filament pointed ends, and ∼80kDa of its C-terminal region integrates within the Z-line lattice. Here, we determined the exon/intron organization of the entire mouse nebulin gene, which contains 165 exons in a 202kb segment. We identified 16 novel exons, 15 of which encode nebulin-repeat motifs (12 from its central region and 3 from its Z-line region). One novel exon shares high sequence homology to the 20 residue repeats of the tight-junction protein, ZO-1. RT-PCR analyses revealed that all 16 novel exons are expressed in mouse skeletal muscle. Surprisingly, we also amplified mRNA transcripts from mouse and human heart cDNA using primers designed along the entire length of nebulin. The expression of cardiac-specific nebulin transcripts was confirmed by in situ hybridization in fetal rat cardiomyocytes and in embryonic Xenopus laevis (frog) heart. On the protein level, antibodies specific for skeletal muscle nebulin's N and C-terminal regions stained isolated rat cardiac myofibrils at the pointed and barbed ends of thin filaments, respectively. These data indicate a conserved molecular layout of the nebulin filament systems in both cardiac and skeletal myofibrils. We propose that thin filament length regulation in cardiac and skeletal muscles may share conserved nebulin-based mechanisms, and that nebulin isoform diversity may contribute to thin filament length differences in cardiac and skeletal muscle. © 2003 Elsevier Science Ltd. All rights reserved.

Schoenwolf, G., Antin, P., Padhye, S., & Pendleton, A. (2008). DD is fully compliant (and then some) with NIH and other funding agencies. Developmental Dynamics, 237(9), 2283-.
Antin, P. B., Pier, M., Sesepasara, T., Yatskievych, T. A., & Darnell, D. K. (2010). Embryonic expression of the chicken Krüppel-like (KLF) transcription factor gene family. Developmental dynamics : an official publication of the American Association of Anatomists, 239(6), 1879-87.

The Krüppel-like transcription factors (KLF) are zinc finger proteins that activate and suppress target gene transcription. Although KLF factors have been implicated in regulating many developmental processes, a comprehensive gene expression analysis has not been reported. Here we present the chicken KLF gene family and expression during the first five days of embryonic development. Fourteen chicken KLF genes or expressed sequences have been previously identified. Through synteny analysis and cDNA mapping, we have identified the KLF9 gene and determined that the gene presently named KLF1 is the true ortholog of KLF17 in other species. In situ hybridization expression analyses show that in general KLFs are broadly expressed in multiple cell and tissue types. Expression of KLFs 3, 7, 8, and 9, is widespread at all stages examined. KLFs 2, 4, 5, 6, 10, 11, 15, and 17 show more restricted patterns that suggest multiple functions during early stages of embryonic development.

Lencinas, A., Broka, D. M., Konieczka, J. H., Klewer, S. E., Antin, P. B., Camenisch, T. D., & Runyan, R. B. (2010). Arsenic exposure perturbs epithelial-mesenchymal cell transition and gene expression in a collagen gel assay. Toxicological sciences : an official journal of the Society of Toxicology, 116(1), 273-85.

Arsenic is a naturally occurring metalloid and environmental contaminant. Arsenic exposure in drinking water is reported to cause cancer of the liver, kidneys, lung, bladder, and skin as well as birth defects, including neural tube, facial, and vasculogenic defects. The early embryonic period most sensitive to arsenic includes a variety of cellular processes. One key cellular process is epithelial-mesenchymal transition (EMT) where epithelial sheets develop into three-dimensional structures. An embryonic prototype of EMT is found in the atrioventricular (AV) canal of the developing heart, where endothelia differentiate to form heart valves. Effects of arsenic on this cellular process were examined by collagen gel invasion assay (EMT assay) using explanted AV canals from chicken embryo hearts. AV canals treated with 12.5-500 ppb arsenic showed a loss of mesenchyme at 12.5 ppb, and mesenchyme formation was completely inhibited at 500 ppb. Altered gene expression in arsenic-treated explants was investigated by microarray analysis. Genes whose expression was altered consistently at exposure levels of 10, 25, and 100 ppb were identified, and results showed that 25 ppb in vitro was particularly effective. Three hundred and eighty two genes were significantly altered at this exposure level. Cytoscape analysis of the microarray data using the chicken interactome identified four clusters of altered genes based on published relationships and pathways. This analysis identified cytoskeleton and cell adhesion-related genes whose disruption is consistent with an altered ability to undergo EMT. These studies show that EMT is sensitive to arsenic and that an interactome-based approach can be useful in identifying targets.