Plant Breeding Laboratory, Faculty of Agriculture, Kyushu University, Fukuoka, 812-8581 Japan

     During the development of a series of chromosome segment substitution lines of Indica rice with the genetic background of Japonica rice (Kubo et a!. 1999), Kubo and Yoshimura (1998) identified a gene causing F2 sterility on chromosome 12. Indica variety IR24 has s(t) allele and Japonica variety Asominori has s+(t) allele. The recessive homozygote s(t)s(t) causes very high spikelet sterility. In this paper, we report identification of the gene complementary to s(t) for the F2 sterility.

     The recombinant inbred lines derived from the cross between Asominori and IR24 (Tsunematsu et al. 1996) were crossed and backcrossed with Asominori (Kubo et a!. 1999). In some populations of BC3F2 generation, we observed the sterile segregants showing approximately 10% spikelet fertility. There were two types of segregation patterns; one was 3:1 segregation and the other was the segregation in which the frequency of sterile plants was significantly lower than 25%. The latter suggested that the sterility may be controlled by two or more genes. The BC3F1 plants which segregated the sterile plants at lower frequency in BC3F2, had a tendency to carry the segment of chromosome 8 from IR24. Therefore, we deduced that the second gene for the sterility was located on chromosome 8.

     To verify the above hypothesis, a BC3F2 plant that was heterozygous for the region of chromosome 8 but homozygous for the region of chromosome 12 from IR24 having the s(t) was selected. In the BC3F3, 54 fertile, 40 semi-sterile and 5 highly sterile plants were observed. At the RFLP locus G104 on chromosome 8, 51 out of 54 fertile plants were homozygous for IR24 alleles, all 39 semi-sterile plants (one of the semi-sterile plants was missed in the RFLP profile) were heterozygous and 4 out of 5 highly sterile plants were homozygous for Asominori alleles. These results demonstrated that Asominori allele at the locus tightly linked to G104 on chromosome 8 is apparently responsible for the F2 sterility and is complementary to IR24 allele at the s(t) locus on chromosome 12. The second gene for F2 sterility was tentatively designated as hsa2(t) (hybrid sterility-a-2) and the previously identified s(t) was renamed hsal(t) (hybrid sterility-a-i). From the results of linkage analysis with RFLP markers, hsa2(t) was located at a distance of 4.7 cM between RFLP markers G104 and C347 on chromosome 8 (Fig. 1).

     In conclusion, the F2 sterility found in the hybrid progeny was controlled by complementary genes, hsai (t) on chromosome 12 and hsa2(t) on chromosome 8. As the genotypes of Asominori and IR24 were hsal+(t)hsal+(t)hsa2(t)hsa2(t) and hsal(t)hsal(t)hsa2(t)+(t)hsa2+(t), the double recessive hsai(t)hsai(t)hsa2(t)hsa2(t) caused high sterility. Previous workers (Oka and Doida 1962, Oka 1978, Yokoo 1984) proposed that F2 sterility was controlled by duplicate genes derived from both parents. Our results supported the previous reports and defined the map position of duplicate genes for F2 sterility based on RFLP analysis.