De Pater Lab
The role of GATA2 in normal and malignant hematopoiesis
Emma (E.M.) de Pater
E-mail: e.depater@erasmusmc.nl
X: @DePaterLab
Scopus: link
Orcid: link
PubMed: link
LinkedIn: link
Contact:
Tessa Mannee, secretary, t.mannee@erasmusmc.nl
![](https://primary.jwwb.nl/public/w/c/c/temp-gcniowhiipjjnutwbwxc/plv660/picemma.jpg?enable-io=true&enable=upscale&crop=1918%2C1880%2Cx1%2Cy0%2Csafe&width=256&height=251)
Emma de Pater studied Biology at the University of Leiden and graduated Sept 30th 2005. June 3rd 2010 she obtained her PhD from Utrecht University after completing her thesis on the growth of the zebrafish heart at the Hubrecht Institute in the group of Prof. Jeroen Bakkers. She started her postdoctoral work in the lab of Prof Elaine Dzierzak at Erasmus MC and investigated the role of the transcription factor Gata2 in the generation of hematopoietic stem cells (HSCs) in the mouse embryo. Here she discovered that GATA2 is required for HSC generation and maintenance at several stages during ontogeny. In 2015 she started her research group, combined with management of the cancer genome editing center, at the department of Hematology investigating the role of GATA2 in leukemia predisposition syndromes. Her group uses mouse-, zebrafish- and cell models to study the effects of GATA2 mutation on normal and malignant hematopoiesis. In 2017 she became assistant professor and since 2020 she combines management of her research group with management of the transplantation laboratory of the department of hematology. The transplantation laboratory is responsible for the processing of stem cell- and lymphocyte products with which over 300 patients are treated annually.
Our research
The de Pater lab studies the role of the transcription factor GATA2 in acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS).
The transcription factor GATA2 is recurrently mutated in AML. Furthermore, the most common germline defect in childhood MDS/AML is a mutation in GATA2. The mutational spectrum of GATA2 in these patients is very diverse, as are the phenotypes of the patients. Some patients have severe hematological deficiencies, while others only have a predisposition for MDS/AML. The reason for this is unknown. These patients have innate mutations in GATA2, which means that these mutations are also present during embryonic development of the hematopoietic system. Innate mutations in Gata2 in mouse and zebrafish result in a severe reduction in the number of HSCs that are generated in the embryo. A novel zebrafish model for GATA2 haploinsufficiency mimics patient characteristics like monocytopenia and dysplasia. The de Pater group is currently investigating the mechanism of malignant transformation in this model and the embryonic role of GATA2 to the contribution of leukemia predisposition. Furthermore, the types of mutations found in de novo AML and in patients with a germline predisposition for MDS/AML are different and how these mutations result in leukemogenesis and deregulate transcription are subject of active investigation.
Our team
Emma de Pater, principal investigator
Mariëtte ter Borg, research technician
Hans de Looper, research technician
Soura Mardpour, postdoc
Wei Zhang, postdoc
Iris Peters, PhD student
Marc Meeuwsen, intern
Alumni
Grigorios Alvanidis
Emanuele Gioacchino
Cansu Koyunlar
![](https://primary.jwwb.nl/public/w/c/c/temp-gcniowhiipjjnutwbwxc/ge61at/dsc02964_groep_emmadepaterjpg.jpg?enable-io=true&enable=upscale&crop=1918%2C1280%2Cx1%2Cy0%2Csafe&width=382&height=255)
Key publications
Koyunlar C, Gioacchino E, Vadgama D, de Looper H, Zink J, Hoogenboezem R, Havermans H, Bindels E, Dzierzak E, Touw IP, Emma de Pater. Gata2-regulated Gfi1b expression controls endothelial programming during endothelial-to-hematopoietic transition Blood adv; 2023, May 23;7(10):2082-2093.
Gioacchino E, Zhang W, Koyunlar C, Zink J, de Looper H, Gussinklo KJ, Hoogenboezem R, Bosch D, Bindels E, Touw IP, Emma de Pater. Gata2b haploinsufficiency causes an epigenetic feedback mechanism resulting in myeloid and erythroid dysplasia BioRxiv, 2021, doi: 10.1101/2021.10.29.466416
Gioacchino E, Koyunlar C, Zink J, de Looper H, de Jong M, Dobrzycki T, Mahony CB, Hoogenboezem R, Bosch D, van Strien P, van Royen E, French PJ, Bindels E, Gussinklo KL, Monteiro R, Touw IP and Emma de Pater. Essential role for Gata2 in modulating lineage output from hematopoietic stem cells identified in zebrafish. Blood Advances. 2021, Jul 13;5(13):2687-2700.
Koyunlar C. and Emma de Pater. From basic biology to patient mutational spectra of GATA2 haploinsufficiencies: What are the mechanisms, hurdles and prospects of genome editing for treatment. Frontiers in Genome Editing. 2020, Nov 26;2:602182.
Dobrzycki T, Mahony CB, Krecsmarik M, Koyunlar C, Rispoli R, Peulen-Zink J, Gussinklo K, Fedlaoui B, Emma de Pater, Patient R, Monteiro R. Deletion of a conserved Gata2 enhancer impairs haemogenic endothelium programming and adult Zebrafish haematopoiesis. Communications Biology. 2020 Feb 13;3(1):71.
Emma de Pater & Trompouki E. Bloody zebrafish – Emerging methods in the study of normal and malignant hematopoiesis. Frontiers in Cell and Developmental Biology. 2018; 6: 124.
Kaimakis P, Emma de Pater, Eich C, Solaimani Kartalaei P, Kauts ML, Vink CS, van der Linden R, Jaegle M, Yokomizo T, Meijer D, Dzierzak E. Functional and molecular characterization of mouse Gata2-independent hematopoietic progenitors. Blood. 2016 Mar 17;127(11):1426-37.
Emma de Pater, Kaimakis P, Vink C, Yokomizo T, Yamada-Inagawa T, Van der Linden R, Camper S, Speck N and Dzierzak E. Gata2 is required for HSC generation and survival. Journal of Experimental Medicine. Journal of Experimental Medicine. 2013 Dec;210(13):2843-50.
Emma de Pater, Ciampricotti M, Priller F, Veerkamp J, Strate I, Smith K, Lagendijk AK, Schilling TF, Herzog W, Abdelilah-Seyfried S, Hammerschmidt M, Bakkers J. Bmp signaling exerts opposite effects on cardiac differentiation. Circ Res. 2012 Feb 17;110(4):578-87
Emma de Pater, Clijsters L, Marques SR, Lin YF, Garavito-Aguilar ZV, Yelon D, Bakkers J. Distinct phases of cardiomyocyte differentiation regulate growth of the zebrafish heart. Development. 2009 May;136(10):1633-41.