Restriction-modification systems and genetic variability of Xanthomonas oryzae pv. oryzae
[Thesis]
S.-H. Choi
J. E. Leach
Kansas State University
1993
170
Ph.D.
Kansas State University
1993
The XorII methyltransferase gene (xorIIM) and very short patch repair endonuclease gene (xorii-vsr) were cloned from Xanthomonas oryzae pv. oryzae, the rice bacterial leaf blight pathogen. The xorIIM encodes a polypeptide of 47 KD and was identified as a monospecific m5cytosine methyltransferase gene. The xorii-vsr encodes a polypeptide of 19.7 KD and the gene is similar in sequence and size to the E. coli vsr gene of the DNA cytosine methylase system (Dcm). A population of X. oryzae pv. oryzae strains from major rice growing countries in Asia was evaluated for the presence or absence of the XorI and XorII restriction-modification (R-M) systems. Four clonal populations with the phenotypes usdXor{\rm I}\sp+{\rm II}\sp+,\, Xor{\rm I}\sp+{\rm II}\sp-,\ Xor{\rm I}\sp-{\rm II}\sp+,usd and usdXor{\rm I}\sp-{\rm II}\sp-usd were distributed in Asia. The XorII R-M system was predominantly found in southeast Asia, whereas the XorI modification system was most prevalent in northeast Asia. DNA polymorphisms were observed between strains in genomic sequences containing the XorII R-M genes; however, most Philippine strains and all the Indonesian and Korean strains had identical patterns. Based on the geographic distribution of both systems and the genome organization around the XorII system, I propose that the XorI system originated in northeast Asia and moved to southeast Asia, while the XorII system originated in southeast Asia. The existence of several phenotypes in some parts of Asia indicate that after movement of the systems the populations remained clonal. A marker-exchange mutant in which the avirulence gene locus avrXa7 was insertionally inactivated was significantly reduced in aggressiveness to susceptible rice cultivars. Aggressiveness was restored by complementation with a plasmid bearing the avrXa7 gene. Thus, avrXa7 codes for not only resistance-gene-specific avirulence function, but also for pathogenicity functions.