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United States Department of Agriculture

Agricultural Research Service

Title: Multiple Upstream Open Reading Frames of the Barley Mla13 Powdery Mildew Resistance Gene Collectively Down-Regulate Translation

Authors
item Halterman, Dennis
item Wise, Roger

Submitted to: Plant and Animal Genome Conference Proceedings
Publication Type: Proceedings
Publication Acceptance Date: January 15, 2005
Publication Date: January 15, 2005
Citation: Halterman, D.A., Wise, R.P. 2005. Multiple Upstream Open Reading Frames Of The Barley Mla13 Powdery Mildew Resistance Gene Collectively Down-Regulate Translation. XIII Plant and Animal Genome Conference Proceedings. p. P729.

Technical Abstract: To protect themselves against pathogen infection, plants have evolved multifarious defense mechanisms that include the production of antimicrobial compounds and hypersensitive cell death. This includes the regulation of expression of resistance proteins, which function to detect pathogen effectors and initiate the defense response. Barley Mla is one of several Ml genes that confer specific resistance to the powdery mildew fungus, Blumeria graminis f. sp. hordei. Mla13 contains a long (523 nt) transcript leader region with three upstream open reading frames (uORFs) and two alternatively spliced introns. The length of the Mla13 uORFs, which encode up to 70 amino acid peptides, are directly influenced by the splicing of these introns. We have used in vivo and in vitro translation assays to show that Mla13 uORFs function cooperatively to down-regulate translation of the parent cistron up to 13-fold. However, resistance conferred by constitutively transcribed Mla appears to be unaffected by removal of these uORFs, signifying that a potential increase in MLA13 protein is innocuous to barley cells. In addition, cells that possess a predicted increase in MLA13 translation via overexpression and uORF mutation retain their requirement for RAR1, suggesting that this increase is not sufficient to overcome the concentration threshold required for activation of resistance in the absence of RAR1.

Last Modified: 10/30/2014
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