ARS | Publication request: POWDERY MILDEW INDUCED MLA MRNAS ARE ALTERNATIVELY SPLICED AND CONTAIN UPSTREAM OPEN READING FRAMES THAT CUMULATIVELY DOWN-REGULATE TRANSLATION

Submitted to: Keystone Symposia
Publication Type: Proceedings
Publication Acceptance Date: March 10, 2003
Publication Date: April 10, 2003
Citation: HALTERMAN, D.A., WISE, R.P. POWDERY MILDEW INDUCED MLA MRNAS ARE ALTERNATIVELY SPLICED AND CONTAIN UPSTREAM OPEN READING FRAMES THAT CUMULATIVELY DOWN-REGULATE TRANSLATION. AVAILABLE FROM: http://www.keystonesymposia.org/Meetings/ViewMeetings.cfm?MeetingID=658. KEYSTONE SYMPOSIA. 2003.

Technical Abstract: In barley, the Mla13 powdery mildew resistance gene confers Rar1-dependent, AvrMla13-specific resistance to Blumeria graminis f.sp. hordei (Bgh). We have identified cDNA and genomic copies of Mla13, and used these as a model for the regulation of host resistance to obligate biotrophic fungi. We demonstrate quantitatively that a rapid increase in the accumulation of Mla transcripts, as well as transcripts of the Mla-signaling genes, Rar1 and Sgt1, is triggered between 16 and 20 hours post inoculation, the same time frame that haustoria of avirulent Bgh make contact with the host cell plasma membrane. Alternative splicing of two introns within the transcript leader region (TLR) of Mla13 can lead to a different number of upstream open reading frames (uORFs) and variability in the size of uORF2. The presence of the Mla TLR, which regulates levels of translated reporter protein, appears to be required for proper activity in vivo since Mla6 with a deleted TLR, under the control of a strong promoter, leads to a loss of resistance specificity. Our results indicate that regulation of Mla transcription is not constitutive and that induction is coordinately controlled by recognition-specific plant factors. The sudden increase in transcription could account for the rapid defense response phenotype conferred by Mla6 and Mla13, while simultaneous control of the amount of protein synthesis would prevent uncontrolled cell death.