A Gene Block Causing Cross-Incompatibility Hidden in Wild and Cultivated Rice

Unidirectional cross-incompatibility was detected in advanced generations of backcrossing between wild (Oryza rufipogon) and cultivated (O. sativa) rice strains. The near-isogenic line (NIL) of T65wx (Japonica type) carrying an alien segment of chromosome 6 from a wild strain gave a reduced seed setting only when crossed with T65wx as the male. Cytological observations showed that abortion of hybrid seeds occurred as a consequence of a failure of early endosperm development followed by abnormalities in embryo development. The genetic basis of cross-incompatibility reactions in the female and male was investigated by testcrosses using recombinant inbred lines (RILs) that were established through dissecting the introgressed segments of wild and cultivated (Indica type) strains. The results revealed that the crossin-compatibility reaction was controlled by Cif in the female and by cim in the male. When the female plant with Cif was crossed with the male plant with cim, a failure of early endosperm development was observed in the hybrid zygotes. Among cultivars of O. sativa, cim was distributed predominantly in the Japonica type but not in the Indica type. In addition, a dominant suppressor, Su-Cif, which changes the reaction in the female from incompatible to compatible was proposed to present near the centromere of chromosome 6 of the Indica type. Further, the death of young F1 zygotes was controlled by the parental genotypes rather than by the genotype of the hybrid zygote itself since all three genes acted sporophytically, which strongly suggests an involvement of parent-of-origin effects. We discuss the results in relation to the origin of a crossing barrier as well as their maintenance within the primary gene pool.

Recombination and disjunction in female germ cells of Drosophila depend on the germline activity of the gene sex-lethal

Gametogenesis in males and females differs in many ways. An important difference in Drosophila is that recombination between homologous chromosomes occurs only in female meiosis. Here, we report that this process relies on the correct functioning of Sex-lethal (Sxl) which is primarily known as the master gene in somatic sex determination. Certain alleles of this gene (Sxl(fs)) disrupt the germline, but not the somatic function of Sxl and cause an arrest of germ cell development during cystocyte proliferation. Using dominant suppressor mutations that relieve this early block in Sxl(fs) mutant females, we discovered additional requirements of Sxl for normal meiotic differentiation of the oocyte. Females mutant for Sxl(fs) and carrying a suppressor become fertile, but pairing of homologous chromosomes and formation of chiasmata is severely perturbed, resulting in an almost complete lack of recombinants and a high incidence of non-disjunction events. Similar results were obtained when germline expression of wild-type Sxl was compromised by mutations in virilizer (vir), a positive regulator of Sxl. Ectopic expression of a Sxl transgene in premeiotic stages of male germline development, on the other hand, is not sufficient to allow recombination to take place, which suggests that Sxl does not have a discriminatory role in this female-specific process. We propose that Sxl performs at least two tasks in oogenesis: an ‘early’ function in formation of the egg chamber, and a ‘late’ function in progression of the meiotic cell cycle, suggesting that both events are coordinated by a common mechanism.