As a female reproductive organ, the ovule plays an important role in reproductive event. The ovule is the site of megasporogenesis, megagametogenesis and fertilization. The genetic mechanism of ovule development in dicots has been studied intensively. Petunia FBP7 and FBP11 are the members of MADS-box gene family. Expression pattern of these two genes and phenotypes of transgenic plants that inhibit these genes constitutively or express these genes ectopically suggest that FBP7 and FBP11 regulate ovule identity (Angenent et al. 1995). In aintegumenta mutant of Arabidopsis, the number of ovules decreases by less than half of wild-type (Elliot et al. 1996). In contrast, the genetic mechanism of ovule development is almost unknown in monocots. Here, we describe a mutant that exhibits a new type of abnormality in ovule development.

We have found a single recessive mutant from R1 plants of rice cv. Nipponbare regenerated from callus suspension culture. We selected the mutant by its low fertility, and then examined the pistil morphology. The mutant showed approximately 87% seed sterility and had no ovule in 85% of the mature pistils (Fig. 1B). Because stamens seemed normal (Fig. 1C), we regarded the mutant as female sterile and named ovuleless (ovl).

The mature ovl pistil had no ovule, so the pistil was empty. To determine whether the ovuleless phenotype was caused by the lack of ovule primordia or its abortion during development, we observed the early stage of ovule development in ovl. The developing flower of wild type had carpel emerging from the lemma side of floral meristem (Fig. 2A), and the remnant of meristem was converted into ovule primordia (Fig. 2B). The ovl flower normally formed carpel, but the meristem did not develop into ovule primordium (Fig. 2D). Even when the carpel encircled the ovule in the wild-type, ovule primordium was not recognized in ovl (Fig. 2C, F). We concluded that the ovuleless phenotype was caused by the lack of ovule primordia.

Other abnormalities were also observed in ovl plant. At a low frequency, the apical meristem aborted in various steps of reproductive phase. Early abortion was observed in the spikelet meristem after the differentiation of rudimentary glume (Fig. 3A). In one case, spikelet meristem degenerated after it differentiated empty glumes (Fig. 3B). Degeneration at the more advanced stage occurred in the floral meristem after the differentiation of lemma (Fig. 3C). These degenerations frequently occurred in the terminal flowers rather than in the basal flowers of primary branches. The ovl panicle had a fewer number of primary branches than that of wild type. Therefore, degeneration probably occur also in rachis meristem. Meristem degeneration was not observed in the vegetative phase.

Ovuleless phenotype is a feature that has not been reported in dicots. Based on ourobservations, we conclude that OVL gene regulates the differentiation of ovule primordia, the initial step of ovule development.

Meristem degeneration in ovl mutant indicates the possibility that OVL gene regulates not only ovule development but also meristem maintenance in the reproductive phase. Recently, Arabidopsis WUSCHEL gene is reported to control ovule development in addition to stem cell regulation (Grofl-Hardt et al. 2002). The same may be true for OVL gene. It is considered that ovule development and meristem maintenance are partly regulated by a common mechanism.

References

Angenent, G. C., J. Franken, M. Busscher, A. van Dijken, J. L. van Went, H.J.M. Dons, and A.J. van Tunen, 1995. A novel class of MADS box genes is involved in ovule development in Petunia. Plant Cell 7: 1569-1582.

Elliott, R.C., A.S. Betzner, E. Huttner, M.P. Oakes, W.Q.J. Tucker, D. Gerentes, P. Perez and D.R. Smyth, 1996. AINTEGUMENTA, an APETALA2-like gene of Arabidopsis with pleiotropic roles in ovule development and floral organ growth. Plant Cell 8: 155-168.

Grofl-Hardt, R., M. Lenhard, and T. Laux, 2002. WUSCHEL signaling functions in interregional communication during Arabidopsis ovule development. Genes Dev. 16: 1129-1138.