- Ph.D. 2001 (Cellular & Molecular Plant Science), Oklahoma State University, Stillwater, Oklahoma.
- M.Phil. 1990 (Plant Physiology), University of Wales, Bangor, UK.
- B.S. 1985 (Biology), Asmara University, Asmara, Ethiopia.
My research focuses on improving resistance of cereals to drought and fungal diseases. Two major research projects are in progress in my lab:
1) Response of the reproductive structures of cereals to drought stress. The reproductive stage of plants is the most sensitive to drought stress. The research in my lab tries to understand how the reproductive stage of cereals responds to drought using barley as a model. The cereal inflorescence (spike) contains many spikelets (florets) that are surrounded by a husk (composed of leaf-like photosynthetic structures known as lemma and palea). The husk protects the developing seed from pathogens and insects. In addition, the husk is photosynthetically active and supplies the developing seed with assimilates (Abebe et al., 2004; Crop Science 44: 942-950). The husk and the awn are drought tolerant. They can supply the developing seed with assimilates during water deficit when most leaves wilt. Understanding how the reproductive structures respond to drought can offer valuable information on how we can improve yield when available water is limiting at the flowering and grain filling stages. We use functional genomics to analyze gene expression at the transcriptome and proteome level in the spike of drought-stressed barley.
2) Enhancing resistance of barley to Fusarium head blight (FHB) or scab disease through genetic engineering. The devastating scab disease of cereals is caused by the fungus Fusarium graminearum. The disease is responsible for huge economic losses to growers in the northern mid-west of the United States. Scab-infected kernels are shriveled and accumulate mycotoxins, such as deoxynevalenol (DON) making them unusable for malting and animal feed. There is no genetic resistance to scab in barley and fungicide treatments are not effective. One alternative strategy to fight the disease is engineering barley with anti-Fusarium genes. To infect the seed, the pathogen must cross the husk and the seed coat (epicarp). Expression of Fusarium resistant genes at the infection route has a great potential to reduce infection. We use a tissue-specific Lem2promoter (Abebe et al., 2006) to target expression of anti-Fusarium genes in the husk and the epicarp of barley.
1. Battelle Applied Research Grant, State of Iowa
2. U.S. Wheat and Barley Scab initiative
3. U.S. Barley Genome Project
4. Faculty Summer Fellowship, University of Northern Iowa
- Abebe T, Melmaiee K, Berg V and Wise RP. 2010. Drought response in the spikes of barley: gene expression in the lemma, palea, awn, and seed. Funct Integr Genomics 10:191-205.
- Abebe T, Wise RP, and Skadsen SW. 2009. Transcriptional profiling established the awn as the major photosynthetic organ of the barley spike while the lemma and the palea primarily protect the seed. Plant Gen 2:247-259.
- Abebe T, Skadsen R, Patel M and Kaeppler H. 2006. The Lem2 gene promoter of barley directs cell- and development-specific expression of gfp in transgenic plants. Plant Biotechn J 4:35-44.
- Abebe T, Skadsen RW and Kaeppler HF. 2005. A proximal upstream sequence controls tissue-specific expression of Lem2, a salicylate-inducible barley lectin-like gene. Planta 221: 170-183.
- Abebe T, Skadsen RW and Kaeppler HF. 2004. Cloning and Identification of Highly Expressed Genes in Barley Lemma and Palea. Crop Sci 44: 942-950.
- Abebe T, Guenzi AC, Martin B and Cushman JC. 2003. Tolerance of mannitol-accumulating transgenic wheat to water stress and salinity. Plant Physiol 131: 1748-1755.
- Skadsen RW, Sathish P, Federico ML, Abebe T, Fu J and Kaeppler HF. 2002. Cloning of the promoter for a novel barley gene, Lem1, and its organ-specific promotion of gfp expression in lemma and palea. Plant Mol Biol 49:545-555.