7. Mapping of the TINY RICE 1 gene, TR1
 

K. ASANO1, K. MIURA1, Y. HASEGAWA1, H. HIROCHIKA2, M. ASHIKARI1, H. KITANO1, M. MATSUOKA1 and Y. R. LIN3

1) Bioscience and Biotechnology Center, Nagoya University, Nagoya, Aichi, 464-8601 Japan
2) Molecular Genetics Department, National Institute of Agrobiological Sciences, Tukuba Ibaraki, 305-8602, Japan
3) Department of Life Science Fu-Jen Catholic University, Hsinchuang, Taipei, 24205 Taiwan


To date, over 60 dwarf genes have been reported in rice (Futsuhara and Kikuchi 1993). Introgression of dwarf alleles into elite cultivars, conferring lodging resistance, is a major task in breeding program since lodging is a common problem in most cereals and various other crops (Kashiwagi and Ishimaru 2004). Consequently, the introgressions of dwarf alleles improve yields, which increase the economic value. Two best famous semi-dwarf genes, sd1 in rice and Rht1 in wheat, dramatically increase rice and wheat production, known as the "Green Revolution" (Sasaki et al. 2002, Peng et al. 1999). Many mutant genes had been cloned and characterized at molecular and biochemical levels (Ashikari et al. 1999, Sasaki et al. 2002, Hong et al. 2003, Itoh et al. 2004). Exploring novel rice mutant genes can be applied not only in breeding programs but also in scientific research.

We had screened a tiny rice dwarf mutant (tr1) which shows abnormal morphology such as narrow and short leaf blade, and dark green phenotypes, from Tos17 mutant lines. The tr1 was

crossed with Kasalath for linkage analysis. Phenotype of the F1 plants shows wild and a 3 to 1 (337 normal and 91 dwarf plants) segregation was observed in the F2 population. These results indicated that tr1 was recessive, and we used 91 recessive homozygous plants for mapping of tr1. Congruently, tr1 was mapped between PCR markers E4443 and RM264 on the long arm of chromosome 8 (Fig. 2), with a 16 cM interval based on the high-density linkage map of RGP (Rice Genome Project, Harushima et al. 1998). We have not investigated linkage between this mutant and insertion of Tos17. Fine mapping of tr1 by using more genetic markers and more recombinants in this region are under progression. Applying positional cloning of tr1 and learn mechanisms that tr1 affects extreme tiny dwarf is our next objective.

Reference

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