Hartman-JohnAssistant Professor

Dept. of Genetics

Contact Information:

Office Address: KAUL 702
Phone: 996-4195
E-mail: jhartman@uab.edu
Websites: School of Medicine Faculty Profile


Duke University, Durham, NC 
BS, Zoology, 1989

University of Alabama at Birmingham
MD, 1996

Post-Graduate Training:

University of Washington, Seattle, WA 
Resident, Internal Medicine, 1995-7

University of Washington, Seattle, WA 
Fellow, Hematology, 1997-2001

Fred Hutchison Cancer Research Center 
Postdoctoral Fellow, Yeast Genetics, 1998-2004

Research Description:

Biological systems are robust, having the capacity to maintain relatively stable phenotypic outputs over a range of perturbing genetic and environmental inputs. Genetic buffering refers to gene activities within a cell that confer phenotypic stability in a particular context. Genetic interactions, defined whenever the phenotype resulting from a chemical or genetic perturbation is dependent upon a particular gene, reveal buffering; examples being chemical sensitivity or synthetic lethality. Research in the lab is focused on global, quantitative analysis of genetic interactions, and understanding how the structure of interaction networks reflects the global organization of gene circuitry that provides cellular robustness.

To measure gene interaction globally, we perturb an array of ~5000 isogenic yeast deletion strains, and use cell proliferation as a phenotypic readout to quantify the interacting effects between the perturbation and deletion at each locus. By varying the type and intensity of perturbation, the resulting selectivity and strengths of interaction are determined, revealing the relative buffering specificity of each gene. Using gene annotation and other bioinformatics resources to analyze the quantitative patterns of gene interaction, testable hypotheses are generated to further understand the molecular basis of the observed interaction networks.

Genes that interact (exacerbate or compensate) with a known genetic or environmental disease-susceptibility factor can act as disease modifiers, contributing to complex disease traits. Systematic, comprehensive, quantitative understanding of how genetic buffering and cellular robustness are achieved in the highly tractable yeast model system is a strategy for understanding complex genotype-phenotype relationships that may exist generally for eukaryotic cells. My lab develops methodologies for global, quantitative analysis of genetic interactions in the complete set of yeast gene deletion strains. These have been initially applied for studying genetic buffering of DNA replication, to understand robustness against perturbations that contribute to cancer and other diseases resulting from deficiencies in DNA metabolism. However, in the future, our plan is to apply them more generally to understand interaction networks that buffer any pathway or cellular processes of interest, focusing on human disease correlates.


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