Organizing Committee


Poster Presentations

Poster Presentations


Use of Medicago truncatula as a model to identify novel sources of resistance to Asian soybean rust

Presenter: S. R. Uppalapati

All authors and affiliations: SRINIVASA RAO UPPALAPATI(1)*, Yasuhiro Ishiga (1), Holger Schultheiss (2), Shipra Mittal, Vanthana Doraiswamy (1) & Kirankumar S Mysore (1)*
(1)Plant Biology Division, Samuel Roberts Noble Foundation, Ardmore, OK 73401, USA; (2) BASF Plant Sci GmbH, Ctr Agr, D-67117 Limburgerhof, Germany

*For correspondence. Email: sruppalapati@noble.org; ksmysore@noble.org

Soybean rust caused by Phakopsora pachyrhizi Sydow is a major concern for soybean producers and there is an increasing demand for identification of durable resistance to soybean rust. Genetic screening approaches in soybean could be limited by the pools of available genotypes and the labor involved in positional or map-based cloning of the identified gene(s) due to the lack of cloning friendly insertion mutant lines. Medicago truncatula is a fast emerging model plant species, especially for legumes, and in our lab we have generated ~15,000 M. truncatula Tnt1 insertion lines with an average of 25 insertions per line and it seems likely that the M. truncatula mutants obtained upon screening for enhanced susceptibility or resistance to P. pachyrhizi would lead to the identification of novel genes that could be utilized for genetic improvement of soybean. Initial characterization of the M. truncatula-P. pachyrhizi incompatible interaction has shown that the fungus forms long germ-tubes and directly penetrate M. truncatula epidermal cells resulting in small necrotic lesions. However, the pathogen failed to sporulate in M. truncatula. Furthermore, transcriptome analysis of the initial stages of interaction suggested the involvement of the secondary metabolites in nonhost resistance response. Taking advantage of this nonhost or incompatible interaction, we have setup a forward-genetic screen to identify M. truncatula genes involved in nonhost resistance to P. pachyrhizi. Screening of more than 700 Tnt1 lines till date identified fifteen mutant phenotypes. These included, a) thirteen lines that supported more penetration with short germ-tubes with lines, b) One resistant line and c) One line that showed increased necrosis. Three interesting candidate genes including, rer (Resistance to ASR infection), ecd (Enhanced necrotic Cell Death to ASR infection) and epr (Enhanced Penetration of ASR) are being further characterized to identify the genes responsible for the phenotype.

                                        Back to Poster Presentations