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 ( 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.


Holtzer, H., Biehl, J., Antin, P., Tokunaka, S., Sasse, J., Pacifici, M., & Holtzer, S. (1983). Quantal and proliferative cell cycles: how lineages generate cell diversity and maintain fidelity.. Progress in clinical and biological research, 134, 213-227.

PMID: 6664999;Abstract:

There are no known differences between the mechanisms that generate diverse differentiation programs in a mosaic embryo such as Caenorhabdites elegans or in a regulative embryo such as a chick. Transit through an invariant sequence of compartments in a lineage is obligatory for a given precursor cell 1) to inherit its differentiation program from its mother, and 2) to transmit to its daughters, by way of a predetermined binary decision, a new differentiation program. The inheritability of a differentiation program must be encoded in a structural molecule. We postulate that during an S period of a quantal cell cycle, chromosomal structures are so altered that a network of genes that could not be transcribed in the mother becomes available for transcription in the daughters. We do not view as a likely possibility the traditional notion that cell-cell or cell-matrix interactions instruct or commit blank, naive cells to transform into cells with unique differentiation programs. From this perspective, we have initiated experiments to determine the minimal rounds of DNA synthesis, following fertilization, that are required to generate founder cells for several major lineages in the chick. Somewhere between the 15th and 18th generations after fertilization erythrogenic hematocytoblasts that are cytokeratin-positive and vimentin- and hemoglobin-negative undergo a quantal cell cycle. Their daughters are cytokeratin-negative and vimentin- and hemoglobin-positive. DNA synthesis, but not cytokinesis, is an obligatory requirement for this switch in differentiation programs. Essentially similar findings are presented for cells in the cardiogenic, neurogenic, melanogenic, and endothelial lineages. There is no evidence that cell-cell or cell-matrix interactions are required for this diversification. Such interactions, however, may be required for the large number of proliferative cell cycles within particular compartments of particular lineages that are characteristic of all growing or expanding systems. With respect to classical "CFU cells" it is of interest that definitive white blood cells have not yet been identified in these cultures. Lastly, the high ratio of primitive red blood cells to non-red blood cells in the first 40 hours of culture is consistent with the notion that the majority of all cells present in the blastodisc at these early stages are in fact already committed to a unipotent erythrogenic lineage [5, 18, 23, 44, 45]. The issue of changing ratios of cells within compartments of a lineage, as well as of cells in different lineages, is much neglected in consideration of (a) normal embryogenesis, (b) cell-renewal in mature organisms and, particularly,

Bobbs, A. S., Saarela, A. V., Yatskievych, T. A., & Antin, P. B. (2012). Fibroblast Growth Factor (FGF) signaling during gastrulation negatively modulates the abundance of microRNAs that regulate proteins required for cell migration and embryo patterning. Journal of Biological Chemistry, 287(46), 38505-38514.

PMID: 22995917;PMCID: PMC3493895;Abstract:

FGF signaling plays a pivotal role in regulating cell movements and lineage induction during gastrulation. Here we identify 44 microRNAs that are expressed in the primitive streak region of gastrula stage chicken embryos. We show that the primary effect of FGF signaling on microRNA abundance is to negatively regulate the levels of miR-let-7b, -9, -19b, -107, -130b, and -218. LIN28B inhibits microRNA processing and is positively regulated by FGF signaling. Gain- and loss-of-function experiments show that LIN28B negatively regulates the expression of miR-19b, -130b, and let-7b, whereas negative modulation of miR-9, -107, and -218 appears to be independent of LIN28B function. PredictedmRNAtargets of the FGF-regulated microRNAs are over-represented in serine/threonine and tyrosine kinase receptors, including ACVR1, ACVR2B, PDGFRA, TGFBR1, and TGFBR3. Luciferase assays show that these and other candidates are targeted by FGF-regulated microRNAs. PDGFRA,a receptor whose activity is required for cell migration through the primitive streak, is a target of miR-130b and -218 in vivo. These results identify a novel mechanism by which FGF signaling regulates gene expression by negatively modulating microRNA abundance through both LIN28B-dependent and LIN28B-independent pathways. © 2012 by The American Society for Biochemistry and Molecular Biology, Inc.

Antin, P. B., Bates, M. A., Zhang, W., Garriock, R. J., & Yatskievych, T. A. (2002). Precocious expression of cardiac troponin T in early chick embryos is independent of bone morphogenetic protein signaling. Developmental Dynamics, 225(2), 135-141.

PMID: 12242713;Abstract:

Cardiac troponin T (cTNT) is a component of the troponin complex, which confers calcium sensitivity to contraction in skeletal and cardiac muscle. Although it is thought that most components of the contractile myofibril are expressed exclusively in differentiated muscle cells, we observed that mRNAs coding for cTNT were detectable in explanted late gastrula mesoderm at least 12 hr before cardiac myocyte differentiation. We therefore conducted a detailed analysis of cTNT gene expression in the early chick embryo. Whole-mount in situ hybridization studies showed that by Hamburger and Hamilton stage 5, cTNT mRNAs are detectable in lateral mesoderm and, by stage 6, are observed throughout the lateral embryonic and extraembryonic mesoderm in a distribution that is much broader than the recognized heart field. As myocardial cell differentiation commences, cTNT transcripts become progressively localized to the forming heart and, by stage 14, are completely restricted to heart muscle cells. Western blot analyses demonstrated that cTNT protein expression is under translational control, as cTNT protein is not detectable until stage 9, concomitant with myocardial cell differentiation. Removal of endoderm at stage 5 had no effect on cTNT mRNA levels, and the bone morphogenetic protein (BMP) inhibitor noggin failed to block cTNT expression, even in the heart-forming region and in cases where heart formation was inhibited. Implantation of noggin-expressing CHO cells at the anterior midline of stage 7 embryos resulted in cardia bifida. These findings demonstrate the precocious, BMP-independent expression of a gene coding for a myofibrillar protein and suggest that an additional regulatory pathway exists for activation of some cardiogenic genes. © 2002 Wiley-Liss, Inc.

Holtzer, H., Forry-Schaudies, S., & Antin, P. (1986). Effects of a phorbol ester (TPA) and a carcinogen (EMS) on myofibrillogenesis. Toxicology and Industrial Health, 2(2), 121-.
Robb, E. A., Antin, P. B., & Delany, M. E. (2013). Defining the Sequence Elements and Candidate Genes for the Coloboma Mutation. PLoS ONE, 8(4).


The chicken coloboma mutation exhibits features similar to human congenital developmental malformations such as ocular coloboma, cleft-palate, dwarfism, and polydactyly. The coloboma-associated region and encoded genes were investigated using advanced genomic, genetic, and gene expression technologies. Initially, the mutation was linked to a 990 kb region encoding 11 genes; the application of the genetic and genomic tools led to a reduction of the linked region to 176 kb and the elimination of 7 genes. Furthermore, bioinformatics analyses of capture array-next generation sequence data identified genetic elements including SNPs, insertions, deletions, gaps, chromosomal rearrangements, and miRNA binding sites within the introgressed causative region relative to the reference genome sequence. Coloboma-specific variants within exons, UTRs, and splice sites were studied for their contribution to the mutant phenotype. Our compiled results suggest three genes for future studies. The three candidate genes, SLC30A5 (a zinc transporter), CENPH (a centromere protein), and CDK7 (a cyclin-dependent kinase), are differentially expressed (compared to normal embryos) at stages and in tissues affected by the coloboma mutation. Of these genes, two (SLC30A5 and CENPH) are considered high-priority candidate based upon studies in other vertebrate model systems. © 2013 Robb et al.