| Budget Amount *help |
¥50,050,000 (Direct Cost: ¥38,500,000、Indirect Cost: ¥11,550,000)
Fiscal Year 2007: ¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2006: ¥8,840,000 (Direct Cost: ¥6,800,000、Indirect Cost: ¥2,040,000)
Fiscal Year 2005: ¥15,600,000 (Direct Cost: ¥12,000,000、Indirect Cost: ¥3,600,000)
Fiscal Year 2004: ¥20,670,000 (Direct Cost: ¥15,900,000、Indirect Cost: ¥4,770,000)
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| Research Abstract |
Dissecting the nature of male-sterility encoding mitochondrial gene(s) and the nuclear genes (named Rf) that suppress male sterility is quite instructive in understanding the mechanism of cytoplasmic male sterility (CMS) in sugar beet. Here we attempted to clone and characterize the Rf1 locus which controls fertility restoration in sugar beet CMS. The results are as follows.
1. We were able to restrict the possible location of the Rf1 locus to a minimum of six BAC clones spanning an interval of about 260kb. The nucleotide sequencing of the 260-kb region revealed 28 ORFs.
2. Among the 28 ORFs, we found four ORFs which are specifically expressed in flower buds and targeted to mitochondria.
3. The four ORFs are adjacent to one another and all code for metalloprotease. We designated the ORFs MPLs. Interestingly, in a nonrestoring (rf1rf1) genotype we identified homologous ORFs that exhibit deletions and are not expressed in flower buds.
4. In situ hybridization analysis demonstrated that expression of MPLs is confined to the tapetal cells of anthers at the microspore tetrad and young microspore stages. Taken together, our observations suggest strongly that MPLs
5. In an attempt to correlate mitochondrial lesions with cellular metabolic processes in sterile anthers, we found an anther-specific lipid transfer protein gene (named LTP).The gene was revealed to be highly expressed in the tapetal cells of fertile anthers at the young microspore stage but not in sterile anthers throughout flower development. It is most likely that the expression of LTP is down-regulated in the tapetum in response to mitochondrial dysfunction and subsequent physiological changes caused by CMS cytoplasm.
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