Forward chemical genetic screens in Arabidopsis identify genes that influence sensitivity to the phytotoxic compound sulfamethoxazole

BMC Plant Biology

Research Article

Pauline W Wang¹  Pauline Fung¹  Yunchen Gong¹  Jianfeng Zhang¹  Darrell Desveaux²  David S Guttman²  Karl J Schreiber³  Ryan S Austin⁴ 

[1] Centre for the Analysis of Genome Evolution & Function, University of Toronto, M5S 3B2, Toronto, ON, Canada;Department of Cell & Systems Biology, University of Toronto, M5S 3B2, Toronto, ON, Canada;Centre for the Analysis of Genome Evolution & Function, University of Toronto, M5S 3B2, Toronto, ON, Canada;Department of Plant & Microbial Biology, University of California, 94720-3102, Berkeley, CA, USA;Southern Crop Protection and Food Research Centre, Agriculture & Agri-Food Canada, N5V 4T3, London, ON, Canada;

关键词: Chemical genomics;    Sulfanilamides;    Arabidopsis thaliana;   

DOI  :  10.1186/1471-2229-12-226

 received in 2012-04-23, accepted in 2012-11-22,  发布年份 2012

来源: Springer

【 摘 要 】

BackgroundThe sulfanilamide family comprises a clinically important group of antimicrobial compounds which also display bioactivity in plants. While there is evidence that sulfanilamides inhibit folate biosynthesis in both bacteria and plants, the complete network of plant responses to these compounds remains to be characterized. As such, we initiated two forward genetic screens in Arabidopsis in order to identify mutants that exhibit altered sensitivity to sulfanilamide compounds. These screens were based on the growth phenotype of seedlings germinated in the presence of the compound sulfamethoxazole (Smex).ResultsWe identified a mutant with reduced sensitivity to Smex, and subsequent mapping indicated that a gene encoding 5-oxoprolinase was responsible for this phenotype. A mutation causing enhanced sensitivity to Smex was mapped to a gene lacking any functional annotation.ConclusionsThe genes identified through our forward genetic screens represent novel mediators of Arabidopsis responses to sulfanilamides and suggest that these responses extend beyond the perturbation of folate biosynthesis.

【 授权许可】

Unknown   
© Schreiber et al.; licensee BioMed Central Ltd. 2012. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.