Author
Jia, Yulin | |
CORRELL, J - UA DEPT PLANT PATH | |
LEE, F - UA RREC | |
Eizenga, Georgia | |
YANG, Y - UA DEPT PLANT PATH | |
Gealy, David | |
VALENT, B - DUPONT | |
ZHU, Q - DUPONT |
Submitted to: Phytopathology
Publication Type: Abstract Only Publication Acceptance Date: 3/7/2001 Publication Date: N/A Citation: N/A Interpretive Summary: Technical Abstract: Rice blast disease caused by Magnaporthe grisea is a major constraint to rice production worldwide. Understanding how plants can detect pathogen molecules then activate resistance systems will aid in genetically engineering new resistance. Resistance to blast disease occurs when the rice Pi-ta protein responds to expression of the fungal avirulence gene AVR-Pita. AVR-Pita ecncodes a putative pre-pro-neutral metalloprotease. AVR-Pita (176) lacks a pre-pro peptide and contains a mature form of the AVR-Pita protein. Pi-ta encodes a putative cytoplasmic protein with a nucleotide binding site (NBS) and a leucine rich domain (LRD). Thus, Pi- ta belongs to a major class of NBS-type resistance genes. A single nucleotide substitution encoding serine in place of alanine 918 in a natural allele of Pi-ta results in loss of resistance. Pi-ta interacts with AVR-Pita (176) in the yeast two-hybrid system and in vitro binding assays. Transient expression of AVR-Pita (176) inside rice cells elicits Pi-ta dependent cell death. These data suggest that Pi-ta is an intracellular receptor that binds to a fungal molecule and then activates its defense system, and A918 in the Pi-ta LRD is critical for recognition. Progress in a joint effort to understand interactions of Pi-ta and AVR-Pita will be reported |