|Kistler, H - Corby|
Submitted to: Genome
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 7/29/2007
Publication Date: 10/13/2007
Citation: Chang, Y., Cho, S., Kistler, H.C., Sheng, H., Muehlbauer, G.J. 2007. Bacterial artificial chromosome-based physical map of gibberella zeae (fusarium graminearum). Genome. 50:954-962. Interpretive Summary: The USDA ARS Cereal Disease Laboratory has played a pioneering role in the complete mapping of the genome of Fusarium graminearum. This is the pathogen that causes scab - currently among the most devastating diseases of wheat and barley. The fungus not only cuts yields of plants, it also affects their quality and produces harmful toxins. In the past 10 years, a widespread epidemic hit barley and wheat country, both here and around the world. Information on the genetic map is being released as fast as possible so it can reach researchers anywhere in the world and immediately help them discover genes they may use to control scab disease. Many Fusarium species can't cause disease so the genetic map will help us to find out which genes make it possible for F. graminearum to cause scab. We are studying altered strains of the fungus that don't form spores or don't cause disease. That will help us find out which genes are needed to form spores and which genes cause the disease. Our overall goal is to find out how this fungus causes scab, how it produces toxins, and what environmental cues trigger scab. From there, we can devise a strategy for preventing the disease. Based on intensive comparisons of our physical map with the genome sequence and genetic map, our new integrated map is highly reliable and useful for a variety of genomics studies.
Technical Abstract: Fusarium graminearum is the primary causal pathogen of Fusarium head blight of wheat and barley, a major disease problem in the wheat and barley growing regions of the world. To accelerate genomic analysis of F. graminearum, we developed a bacterial artificial chromosome (BAC)-based physical map and integrated it with the genome sequence and genetic map. Two complementary BAC libraries were developed and used to construct the physical map. One library, developed in the HindIII restriction enzyme site consists of 4,608 clones of approximately 107kb insert size and covers about 13.5 genome equivalents. The other library, developed in the BamHI restriction enzyme site consists of 3,072 clones of approximately 95 kb and covers about 8.0 genome equivalents. Combined, these libraries cover approximately 21.5 genome equivalents. We fingerprinted 4,224 BAC clones, 2,688 from the HindIII library and 1,536 from the BamHI library, for an estimated 11.9-fold coverage of the genome. Fingerprint data was used to develop a physical map of F. graminearum consisting of 26 contigs covering 39.2 Mb in length. For confirming the reliability of this physical map, we compared our map to the F. graminearum genome sequence. The comparison shows that the size of our physical map is equivalent to the 36 Mb genome sequence. We used 31 sequence-based genetic markers, randomly spaced throughout the genome, to integrate the physical map with the genetic map. We also BAC-end sequenced 17 BamHI clones and identified four clones that spanned gaps in the genome sequence. Based on intensive comparisons of our physical map with the genome sequence and genetic map, our new integrated map is highly reliable and useful for a variety of genomics studies.