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United States Department of Agriculture

Agricultural Research Service

Title: Chromosome Complement of the Fungal Plant Pathogen Fusarium Graminearum Based on Genetic and Physical Mapping and Cytological Observations

Authors
item Gale, Liane
item Bryant, Je'nise - UNIVERSITY OF MINNESOTA
item Calvo, Sarah - BROAD INSTITUTE, MIT
item Giese, Henriette - KVL, DENMARK
item Katan, Talma - VOLCANI CENTER, ISRAEL
item O`donnell, Kerry
item Suga, Haruhisa - GIFU UNIVERSITY, JAPAN
item Taga, Masatoki - OKAYAMA UNIVERSITY, JAPAN
item Usgaard, Thomas
item Ward, Todd
item Kistler, H

Submitted to: Genetics
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: July 13, 2005
Publication Date: November 1, 2005
Citation: Gale, L.R., Bryant, J., Calvo, S., Giese, H., Katan, T., O Donnell, K., Suga, H., Taga, M., Usgaard, T.R., Ward, T.J., Kistler, H.C. 2005. Chromosome complement of the fungal plant pathogen Fusarium graminearum based on genetic and physical mapping and cytological observations. Genetics. 171:985-1001.

Interpretive Summary: ARS has played a pioneering role in the complete mapping of the genome of Fusarium graminearum. This is the pathogen that causes scab—the most devastating disease of wheat and barley to date. This 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. We know where only half the genes that produce the toxins are. We are now using the genome sequence to find the other ones. 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. It's a case of getting to know your enemy. http://www.ars.usda.gov/is/AR/archive/feb05/fusarium0205.htm

Technical Abstract: In order to validate and augment the draft whole genome sequence assembly of the filamentous fungus, Fusarium graminearum, a genetic map was constructed. A mapping population was created from a cross between the sequenced strain (PH-1 =NRRL 31084) and a field strain from Minnesota (00-676 =NRRL 34097). A total of 111 ascospore progeny were analyzed for segregation at 235 loci. Genetic markers consisted of sequence-tagged sites, primarily detected as dCAPs or CAPs (n=131) and VNTRs (n=31), AFLPs (n=66), and seven other markers. While most markers exhibited Mendelian inheritance, segregation distortion was observed for 25 predominantly clustered markers. A linkage map was generated using the Kosambi mapping function in JoinMap 3.0 using a LOD threshold value of 3.5. Nine linkage groups were detected covering 1234 cM and anchoring 99.83% of the draft sequence assembly. All 9 linkage groups and 22 anchored scaffolds from the sequence assembly were assembled into 4 chromosomes, leaving only 5 smaller scaffolds (52,630 bp total) of the nuclear DNA unanchored. A chromosome number of four was confirmed by cytological karyotyping. Further analysis of the genetic map data identified variation in recombination rate in different genomic regions that often spanned several hundred kb.

Last Modified: 10/24/2014
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