LOCATION: University of Wisconsin-Madison


The Bresnick laboratory is recruiting a postdoctoral trainee to work on normal and malignant hematopoiesis, as well as fundamental problems in cellular regulation, including epigenetics. The laboratory is located in the new Wisconsin Institute of Medical Research (WIMR) research facility in the UW School of Medicine and Public Health, which provides a highly collaborative scholarly environment for conducting innovative basic and translational/clinical research.

We use multidisciplinary approaches to understand biological and mechanistic processes, including stem/progenitor cell function, blood cell development, and pathologies including cancer, myelodysplastic syndromes and anemia. These studies involve genomics, proteomics, gene editing, computational analysis, and powerful molecular, cellular, and biochemical methodologies in primary cells and mice. Postdoctoral trainees have ample opportunities to develop high-impact research projects in these areas, gain expertise in fellowship/grant writing, and hone their critical thinking and presentation skills to prepare for careers in academia, private sector or other venues.

Research Topics include:

  • Hematopoiesis and Disease Mechanisms. Deviations from hematopoietic programs yield leukemia, lymphoma, myelodysplastic syndromes and anemias. We are analyzing GATA transcription factor mechanisms that suppress or cause pathologies and are using these mechanisms to forge translational/clinical
  • Epigenetic Mechanisms and Synthetic We are addressing mechanistic and translational issues in genome biology, e.g. how cis-elements function in chromatin, how genetic networks are established and maintained and how chromatin modification/remodeling regulate transcription of endogenous loci.


The successful candidate shall hold a PhD from an excellent university, have no more than three prior years of postdoctoral experience, have published at least one important first-author paper from their doctoral research and have excellent communication/interaction skills.


Apply via email to:  Emery H. Bresnick, Ph.D.,


Churpek et al. (2019) Transcription factor mutations as a cause of myeloid neoplasms. J. Clin. Invest.


Soukup et al. (2019) Single-nucleotide human disease mutation inactivates a blood-regenerative GATA2 enhancer. J. Clin. Invest.


Katsumura et al. (2018) Human leukemia mutations corrupt but do not abrogate GATA2 function. Proc. Natl. Acad. Sci. U.S.A. Tanimura et al. (2018) GATA/heme multi-omics reveals a trace metal-dependent cellular differentiation mechanism. Dev. Cell Mehta et al. (2017) Integrating enhancer mechanisms to establish a hierarchical blood development program. Cell Rep.

Hewitt et al. (2017) GATA factor-regulated Samd14 enhancer confers red blood cell regeneration and survival in severe anemia. Dev Cell.


Katsumura KR et al. GATA Factor Mechanisms Group. (2017) The GATA factor revolution in hematology. Blood


McIver et al. (2016) Exosome complex orchestrates developmental signaling to balance proliferation and differentiation during erythropoiesis. Elife


Johnson et al. (2015) Cis-regulatory mechanisms governing stem and progenitor cell transitions. Sci Advances


Hewitt et al. (2015) Hematopoietic signaling mechanism revealed from a stem/progenitor cell cistrome. Mol. Cell


Katsumura et al. Molecular basis of crosstalk between oncogenic Ras and the master regulator of hematopoiesis GATA-2. EMBO Rep. 2014 Sep;15(9):938-47.


Yamazaki et al. (2014) A remote GATA2 hematopoietic enhancer drives leukemogenesis in inv(3)(q21;q26) by activating EVI1 expression. Cancer Cell


Gao X et al. (2013) Gata2 cis-element is required for hematopoietic stem cell generation in the mammalian embryo. J. Exp. Med.


Johnson et al. (2012) Cis-element mutated in GATA2-dependent immunodeficiency governs hematopoiesis and vascular integrity. J. Clin. Invest.


Fujiwara et al. (2009) Discovering hematopoietic mechanisms through genome-wide analysis of GATA factor chromatin occupancy. Mol. Cell