Amanda L. Zacharias, PhD
- Member, Division of Developmental Biology
- Assistant Professor, UC Department of Pediatrics
About
Biography
I'm a research biologist aiming to understand how an embryo develops: its gene expression, cell signaling, cell shape changes and cell migrations. In my lab, we're interested in how cellular metabolism impacts these processes and how vitamins influence cellular metabolism in embryos.
To study the functions of cellular metabolism, we aim to understand the embryonic development of a simple animal completely using time-lapse imaging. We utilize the organism Caenorhabditis elegans (C. elegans) because they are fast, inexpensive and simple, so we study their development more comprehensively. We are interested in how environmental factors might impact different developmental processes, and we recently found that vitamin B12 significantly improves cell migration and embryo survival in a class of developmental mutants.
One of our groundbreaking discoveries occurred using time-lapse imaging. We discovered that cells have a stronger response to a Wnt signal if they received a previous Wnt signal (Zacharias et al. 2015).
I'm thankful to have received a K99/R00 grant to help fund my research. I have been a research biologist for over twenty years and began working at Cincinnati Children's in 2018. See my current lab website for more about our research and why we study C. elegans at a children's hospital. https://www.cincinnatichildrens.org/research/divisions/d/dev-biology/labs/zacharias/model
BS: Biomedical Engineering, Northwestern University, Evanston, IL, 2003,
PhD: Cell and Developmental Biology, University of Michigan, Ann Arbor, MI, 2009,
Postdoctoral Fellow: Ophthalmology, University of Michigan, Ann Arbor, MI, 2009-2011,
Postdoctoral Fellow: Genetics, University of Pennsylvania, Philadelphia, PA, 2011-2018,
Interests
Embryonic metabolism; morphogenesis; Caenorhabditis elegans
Research Areas
Publications
Vitamin B12 partially rescues embryonic cell migration defects in Caenorhabditis elegans ephrin mutants by improving propionic acid breakdown and one-carbon cycle metabolism. Genetics. 2025; 230(2).
pop-1/TCF, ref-2/ZIC and T-box factors regulate the development of anterior cells in the C. elegans embryo. Developmental Biology. 2022; 489:34-46.
The anterior Hox gene ceh-13 and elt-1/GATA activate the posterior Hox genes nob-1 and php-3 to specify posterior lineages in the C. elegans embryo. PLoS Genetics. 2022; 18(5):e1010187.
De Novo-Designed Near-Infrared Nanoaggregates for Super-Resolution Monitoring of Lysosomes in Cells, in Whole Organoids, and in Vivo. ACS Nano. 2019; 13(12):14426-14436.
β-catenin is required in the neural crest and mesencephalon for pituitary gland organogenesis. BMC Developmental Biology. 2016; 16(1):16.
Combinatorial decoding of the invariant C. elegans embryonic lineage in space and time. Genesis (United States). 2016; 54(4):182-197.
Overlapping cell population expression profiling and regulatory inference in C. elegans. BMC Genomics. 2016; 17:159.
Quantitative Differences in Nuclear β-catenin and TCF Pattern Embryonic Cells in C. elegans. PLoS Genetics. 2015; 11(10):e1005585.
The Bicoid class homeodomain factors ceh-36/OTX and unc-30/PITX cooperate in C. elegans embryonic progenitor cells to regulate robust development. PLoS Genetics. 2015; 11(3):e1005003.
The homeodomain transcription factor PITX2 is required for specifying correct cell fates and establishing angiogenic privilege in the developing cornea. Developmental Dynamics. 2014; 243(11):1391-1400.
3333 Burnet Avenue, Cincinnati, Ohio 45229-3026
© 1999-2025 Cincinnati Children's Hospital Medical Center. All rights reserved.
