|1988-1993 Indiana University in Bloomington, Indiana, USA
BS in Biology, BS in Music and outside field (Chemistry)
1993-1994 Fulbright Scholar, Albrecht Ludwigs Universität Freiberg, Freiberg, Germany.
1993-1995 Research Student, Max-Planck Institute for Immunology, Freiburg, Germany.
1996-2003 PhD, UT Southwestern Medical Center at Dallas, Texas, USA
2003-2007 Post-doctoral Fellow, Max-Planck Institute for Developmental Biology, Tübingen, Germany.
2008-2015 Group Leader, DFG-Center for Regenerative Therapies Dresden, Technische Universität Dresden, Dresden, Germany
2015-2016 Group Leader, Department of Pharmacology and Toxicology, Medizisch-Theoretisches Zentrum, Technische Universität Dresden, Dresden, Germany.”
2016-present adjunct affiliation with Department of Pharmacology and Toxicology, Medizisch-Theoretisches Zentrum, Technische Universität Dresden, Dresden, Germany.
2016-present Associate Professor, PI, School of Life Sciences and Technology, ShanghaiTech, Shanghai, China
|The Antos group researches tissue regeneration. To understand the biology of regeneration, Dr. Antos is interested in answering three fundamental questions:
1. How are cells at the site of injury induced to regenerate lost tissues?
2. How are cells involved in regeneration controlled to produce the correct pattern?
3. What stops regeneration once the appropriate size is reached?
These questions are highly relevant to tissue bioengineering and to the stem cell biology of repair or reconstruction of human tissues. The Antos lab uses the zebrafish to answer these questions, because the zebrafish will regenerate many of its organs, including heart and appendages. Therefore, the lab can describe and dissect the cell and molecular mechanisms involved in the fish’s regeneration abilities and relate them to the limits on mammalian regeneration.
Although the zebrafish fins have different architectures to the mammalian limbs, they contain almost all the same tissue types (bone, mesenchyme, joints, skin, melanocytes, etc.). These tissues just are arranged in a different pattern. Unlike mammalian limbs, after partial loss, the zebrafish fin will regenerate completely. Because the zebrafish can be researched with the current cell, genetic and molecular research tools, this regeneration model allows the Antos lab to assess the mechanisms involved in how to start, pattern and stop the stem and progenitor cells involved in regenerating appendages.
Healthy heart physiology requires coordinated Ca2+ handling across the syncytial cardiac muscle. While single-cell cardiomyocyte experiments in culture indicate how individual cardiomyocytes alter their Ca2+ subcellular distribution and handling properties, they are limited in addressing the syncytial nature of the cardiomyocytes in the heart in vivo. Thus, experimental dissection at the organ, cell and molecular levels are needed to understand how known and to-be-discovered mechanisms regulate cardiac physiology during heart regeneration in vivo. The Antos lab is therefore using all the current cell and molecular methods, including real-time in vivo zebrafish heart imaging, to address fundamental questions about cardiac injury, regeneration and function.
1. Antos CL, Knopf F & Brand M. (2015) Encyclopedia Article: “Regeneration of Organs and Appendages in Zebrafish: A Window into Underlying Cellular and Molecular Control Mechanisms”, Encyclopedia of Life Sciences, http://www.els.net/
2. Kujawski S, Lin W, Kitte F, Börmel M, Fuchs S, Arulmozhivarman G, Vogt S, Theil D, Zhang Y & Antos CL (2014) Calcineurin regulates coordinated outgrowth of zebrafish regenerating fins. Developmental Cell 28: 573-587
3. Kizil C, Küchler B, Yan J-J, Özhan G, Moro E, Argenton F, Brand M, Weidinger G & Antos CL (2014) Simplet/Fam53b (Smp) is required for Wnt signal transduction by regulating β-catenin nuclear localization. Development 141: 3529-3539.
4. Kizil C, Otto GW, Geisler R, Nüsslein-Volhard C & Antos CL, (2009) Simplet controls cell proliferation and gene transcription during zebrafish caudal fin regeneration. Dev. Biol. 325: 329-340.
5. Antos CL, Lopez-Rodriguez C, Shelton JM, Richardson JA, Lin F, Novobrantseva TI, Bronson RT, Igarashi P, Rao A & Olson EN. (2004) Loss of NFAT5 results in renal atrophy and lack of tonicity-responsive gene expression Proc. Natl. Acad. Sci. U.S.A. 101: 2392-2397.
6. Antos CL, McKinsey TA, Dreitz M, Hollingsworth LM, Zhang CL, Schreiber K, Rindt H & Olson EN. (2003) Dose-Dependent Blockade to Cardiomyocyte Hypertrophy by Histone Deacetylase Inhibitors J. Biol. Chem. 278: 28930-28937.
7. Antos CL, McKinsey TA, Frey N, Kutschke W, McAnally J, Shelton JM, Richardson JA, Hill JA & Olson EN. (2002) Activated Glycogen Synthase [Kinase]-3β Suppresses Cardiac Hypertrophy in vivo. Proc. Natl. Acad. Sci. U.S.A. 99: 907-912.
8. Antos CL, Frey N, Marx SO, Reiken S, Gaburjakova M, Richardson JA, Marks AR & Olson EN. (2001) Dilated Cardiomyopathy and Sudden Death Resulting from Constitutive Activation of Protein Kinase A. Circ. Res. 89: 997-1004.