Bacterial blight caused by Xanthomonas oryzae pv. oryzae (Xoo) is a chief factor limiting rice productivity worldwide. XM14, a rice mutant line resistant to Xoo, has been obtained by treating IR24, which is susceptible to six Philippine Xoo races and six Japanese Xoo races, with N-methyl-N-nitrosourea. XM14 showed resistance to six Japanese Xoo races. The F2 population from XM14 × IR24 clearly showed 1 resistant : 3 susceptible segregation, suggesting control of resistance by a recessive gene. The approximate chromosomal location of the resistance gene was determined using 10 plants with shortest lesion length in the F2 population from XM14 × Koshihikari, which is susceptible to Japanese Xoo races. DNA marker-assisted analysis revealed that the gene was located on chromosome 3. IAS16 line carries IR24 genetic background with a Japonica cultivar Asominori segment of chromosome 3, on which the resistance gene locus was thought to be located. The F2 population from IAS16 × XM14 showed a discrete distribution. Linkage analysis indicated that the gene is located around the centromeric region. The resistance gene in XM14 was a new gene, named XA42. This gene is expected to be useful for resistance breeding programs and for genetic analysis of Xoo resistance.

Background: The perennial, Oryza rufipogon distributed from Asia to Australia and the annual O. meridionalis indigenous to Australia are AA genome species in the Oryza. However, recent research has demonstrated that the Australian AA genome perennial populations have maternal genomes more closely related to those of O. meridionalis than to those found in Asian populations of O. rufipogon suggesting that the Australian perennials may represent a new distinct gene pool for rice. Results: Analysis of an Oryza core collection covering AA genome species from Asia to Oceania revealed that some Oceania perennials had organellar genomes closely related to that of O meridionalis (meridionalis-type). O. rufipogon accessions from New Guinea carried either the meridionalis-type or rufirpogon-type (like O. rufipogon) organellar genomes. Australian perennials carried only the meridionalis-type organellar genomes when accompanied by the rufipogon-type nuclear genome. New accessions were collected to better characterize the Australian perennials, and their life histories (annual or perennial) were confirmed by field observations. All of the material collected carried only meridionalis-type organellar genomes. However, there were two distinct perennial groups. One of them carried an rufipogon-type nuclear genome similar to the Australian O. rufipogon in the core collection and the other carried an meridionalis-type nuclear genome not represented in the existing collection. Morphologically the rufipogon-type shared similarity with Asian O. rufipogon. The meridionalis-type showed some similarities to O. meridionalis such as the short anthers usually characteristic of annual populations. However, the meridionalis-type perennial was readily distinguished from O. meridionalis by the presence of a larger lemma and higher number of spikelets. Conclusion: Analysis of current accessions clearly indicated that there are two distinct types of Australian perennials. Both of them differed genetically from Asian O. rufipogon. One lineage is closely related to O. meridionalis and another to Asian O. rufipogon. The first was presumed to have evolved by divergence from O. meridionalis becoming differentiated as a perennial species in Australia indicating that it represents a new gene pool. The second, apparently derived from Asian O. rufipogon, possibly arrived in Australia later.

Hybrid weakness phenomena in rice reportedly have two causes: those of HWC1 and HWC2 genes and those of HWA1 and HWA2 genes. No detailed study of the latter has been reported. For this study, we first produced crosses among cultivars carrying the weakness-causing allele on the HWA1 and HWA2 loci to confirm the phenotype of the hybrid weakness and the genotypes of the cultivars on the two loci, as reported earlier. We then confirmed that these cultivars belong to Indica. Subsequent linkage analysis of HWA1 and HWA2 genes conducted using DNA markers revealed that both genes are located in the 1,637-kb region, surrounded by the same DNA markers on the long arm of chromosome 11. The possibility of allelic interaction inducing hybrid weakness is discussed.

Hybrid weakness is a reproductive barrier. In rice, the hybrid weakness caused by two complementary genes––HWC1 and HWC2––has been surveyed extensively. However, their gene products and the molecular mechanism that causes hybrid weakness have remained unknown. We first performed fine mapping of HWC2, narrowing down the area of interest to 19 kb. We thereby identified five candidate genes. Second, we performed haplotype analysis around the HWC2 locus of 33 cultivars. With 15 DNA markers examined, all the 13 Hwc2-1 carriers share the same haplotype for consecutive 14 DNA markers. As for hwc2-2 carriers, five out of 20 have the haplotypes relatively similar to those of Hwc2-1 carriers. However, the other haplotypes differ remarkably from them. These results are useful to identify the HWC2 gene and to study rice varietal differentiation.

Many postzygotic reproductive barrier forms have been reported in plants: hybrid weakness, hybrid necrosis, and hybrid chlorosis. In this study, linkage analysis of the genes causing hybrid chlorosis in F₂generation in rice,HCA1andHCA2, was performed.HCA1andHCA2are located respectively on the distal regions of the short arms of chromosomes 12 and 11. These regions are known to be highly conserved as a duplicated chromosomal segment. The molecular mechanism causing F₂chlorosis deduced from the location of the two genes was discussed. The possibility of the introgression of the chromosomal segments encompassingHCA1and/orHCA2was also discussed from the viewpoint of Indica-Japonica differentiation.