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United States Department of Agriculture

Agricultural Research Service

Title: The Rf2 Nuclear Restorer of Male-Sterile, T-Cytoplasm Maize Encodes An Aldehyde Dehydrogenase

Authors
item Cui, X - ISU
item Liu, F - ISU
item Chen, W - ISU
item Gobelman Werner, Karin
item Wise, Roger
item Schnable, Patrick - ISU

Submitted to: Maize Genetics Conference Abstracts
Publication Type: Abstract Only
Publication Acceptance Date: March 18, 1996
Publication Date: N/A

Technical Abstract: Cytoplasmic male sterility (cms) is a maternally inherited inability to produce functional pollen. In many cms systems, restoration of male fertility can occur in the presence of specific nuclear genes. These fertility-restorer genes are thought to block or compensate for cytoplasmic dysfunctions that are phenotypically expressed during pollen development. Efforts to characterize the molecular mechanisms by which these events occur have been hampered by the complete absence of cloned nuclear restorer genes. Rf2 is one of two complementary nuclear restoration genes of the male-sterile, T cytoplasm of maize. Transposon-tagged rf2-m alleles have been isolated previously. Using these mutant alleles the rf2 gene has been cloned (Cui, Wise and Schnable, Science, 1996). A 2193 bp full-length Rf2 cDNA obtained from a seedling library exhibits 70% amino acid sequence similarity to mammalian mitochondrial aldehyde dehydrogenases (ALDH). This finding has led to the development of two models to explain the role of Rf2 in fertility restoration. The Rf2 cDNA has been expressed in E. coli and the corresponding 60-kDa protein purified. Northern analyses of total RNA from young tassels demonstrated that most rf2 mutants block the accumulation of detectable levels of the rf2 transcript. T-cytoplasm plants homozygous for these rf2-m mutant alleles are male sterile, whereas N-cytoplasm plants with these genotypes are male fertile. Sequence analysis of a genomic clone from the inbred line B73 has established the rf2 gene is more than 19 kb in size.

Last Modified: 12/19/2014
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