Ben F. Holt III

Assistant Professor, Plant Molecular Biology


Dr. Ben Holt

Contact Information:

Ben F. Holt III
219 George Lynn Cross Hall
Office Phone: (405)325-9018
benholt@ou.edu

Education:

Postdoctoral Training: University of North Carolina-Chapel Hill, 2002-2006
PhD in Biology: University of North Carolina-Chapel Hill, 2002
MS in Plant Biology: Ohio University, 1996
BS in Wildlife and Fisheries Management: Frostburg State University, 1990

Research Interests:

Utilizing the fully sequenced model plant Arabidopsis thaliana, our research program is devoted to investigating several families of specialized proteins called transcription factors. Simplified, transcription factors can be imagined as controlling the on/off switches for individual genes – in other words, transcription factors control gene expression. Adding complexity to this simple description, transcription factors cooperate with many other cis and trans acting factors in the cell and often regulate gene expression in subtle ways. During developmental changes, such as the shift from vegetative growth to flowering in plants, expression levels can change for hundreds to thousands of genes. Because transcription factors are one of the major workhorses controlling these global changes in gene expression, understanding their specific functions will yield great insights into plant development and plant responses to environmental fluctuations.

Our work is currently focused on the CCAAT (pronounced “CAT”) box binding transcription factor complex (CBF). CBF complexes are found in all eukaryotes, including yeast, mammals, and plants. A CBF is composed of three subunits (CBF-A, CBF-B, and CBF-C) that assemble in a strict, stepwise fashion.

The resulting CBF heterotrimer binds DNA at CCAAT nucleotide sequences in promoter regions directly upstream of transcription initiation sites. CBF-dependent gene activation can be tissue specific, developmentally regulated, or constitutive. Moreover, approximately 30% of all human genes are thought to have CCAAT elements in their promoters. Despite the wide cellular distribution and functional variability of target genes regulated by CBF, most eukaryotic genomes have only one or two genes encoding each CBF subunit. For example, the Drosophila and C. elegans genomes each encode a total of 6 CBF protein subunits. Humans and mice encode only one copy of each subunit; thus, there is no combinatorial diversity in the subunit composition of the heterotrimeric mammalian CBF.

In striking contrast to mammals, Arabidopsis has 36 CBF genes (13 CBF-A homologs, 10 CBF-B, 13 CBF-C). Agronomically important crop species, such as rice and tomato, also appear to have undergone similar expansions in the number of CBF subunit encoding genes. Because CBF is composed of three subunits, the 36 proteins in Arabidopsis can theoretically be combined to generate ~1,700 unique CBFs! Our initial investigations of Arabidopsis CBF subunit genes have demonstrated that there is considerable variation in their quantitative, developmental, and tissue specific expression patterns.

We can infer from this information that plant CBFs will control target gene expression during many developmental time points in varying tissue types, although very little is currently known regarding these transcription factors. An important goal for our lab is to begin sorting through the possible CBF combinations and identifying their importance in plant development.


Recent Publications:

  1. Kaminaka, H., C. Näke, P. Epple, J. Dittgen, K. Schütze, C. Chaban, B. F. Holt III, T. Merkle, E. Schäfer, K. Harter, and J. L. Dangl. 2006. bZIP10-LSD1 antagonism modulates basal defense and cell death in Arabidopsis following infection. EMBO Journal, in press. (PDF)
  2. Holt III, B.F., Y. Belkhadir, and J.L. Dangl. 2005. Antagonistic control of disease resistance protein stability in the plant immune system. Science, 309: 929-932. Published online 23 June 2005 (PDF)
  3. Kawasaki, T., J. Nam, D. C. Boyes, B. F. Holt III, D. A. Hubert, A. Wiig, and J. L. Dangl. 2005. A duplicated pair of Arabidopsis RING-finger E3 ligases contribute to RPM1- and RPS2-mediated hypersensitive response. Plant Journal, 44: 258-270. Published online 20 September 2005 (PDF)
  4. Mims, C.W., E.A. Richardson, B. F. Holt III, J.L. Dangl. 2004. Ultrastructure of the host-pathogen interface in Arabidopsis thaliana leaves infected by the downy mildew Hyaloperonospora parasitica. Canadian Journal of Botany 82: 1001-1008 (PDF)
  5. Nimchuk, Z., T. Eulgem, B. F. Holt III, J.L. Dangl. 2003. Recognition and response in the plant immune system. Annual Review in Genetics 37: 579-609 (PDF)
  6. Holt III, B.F., D.A. Hubert, and J.L. Dangl. 2003. Resistance gene signaling in plants - Complex similarities to animal innate immunity. Current Opinions in Immunology 15:20-25 (PDF)
  7. Holt III, B.F., Boyes, D.C., Ellerström, M., Siefers, N., Wiig, A., Kauffman, S., Grant, M.R., Dangl, J.L. 2002. An evolutionarily conserved mediator of plant disease resistance gene function is required for normal Arabidopsis development. Developmental Cell 2:1-20 (PDF)
  8. Mackey, D., Holt III, B.F., Wiig, A., Dangl, J.L. 2002. RIN4 interacts with Pseudomonas syringae type III effector molecules and is required for RPM1-mediated resistance in Arabidopsis. Cell 108:743-754 (PDF)
  9. Aviv, D.H., Rustérucci, C., Holt III, B.F., Dietrich, R.A., Parker, J.E., Dangl, J.L. 2002. Runaway cell death, but not basal disease resistance, in lsd1 is SA- and NIM1/NPR1-dependent. Plant Journal 29:381-391 (PDF)
  10. Rustérucci, C., Aviv, D.H., Holt III, B.F., Dangl, J.L., and Parker, J.E. 2001. The disease resistance signaling components EDS1 and PAD4 are essential regulators of the cell death pathway controlled by LSD1 in Arabidopsis. Plant Cell 13:2211-2224 (PDF)
  11. Holt III, B.F., Mackey, D., and Dangl, J.L. 2000. Recognition of pathogens by plants – Primer. Current Biology 10:R5-R7 (PDF)

    For more information about this program, contact the Department or Dr. Ben Holt.


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