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United States Department of Agriculture

Agricultural Research Service


item Lilly, J W
item Havey, Michael

Submitted to: International Plant and Animal Genome IX Conference
Publication Type: Abstract Only
Publication Acceptance Date: 1/15/2001
Publication Date: N/A
Citation: N/A

Interpretive Summary:

Technical Abstract: Mitochondrial mutants are rare due to the importance of respiration and the relatively few mitochondrially encoded products. The mitochondrial genome of cucumber is unique because of its huge size and paternal transmission. We investigated a paternally transmitted mosaic (MSC) phenotype in cucumber. Transmission studies eliminated segregation of a recessive allele conditioning paternal imprinting, but low levels (less than 1 percent) of wild type testcross progenies were documented. We identified a 16 kb deletion (JLV5-DEL) in the mitochondrial genome that was shared among three independently derived MSC lines. This deletion was transmitted with the MSC phenotype through the F3 and testcross generations. The deletion is 4 kb from t-RNA-His and 18 kb from apocytochrome b (cob). PCR amplification using two primer sets for regions within JLV5-DEL revealed that rare wild type sorters possessed this region, and PCR using mtDNA as target revealed low levels (less than 0.5 percent) of the wild type region in MSC16. Therefore, MSC plants are heteroplasmic for the deleted region, but at levels below detection by standard PCR and Southern hybridizations using genomic DNA. The mitochondrial deletion in MSC lines may have been generated in tissue culture by recombination among short direct (tandem) repeats at the ends of the deleted region. Sequence analyses revealed no homologies to mitochondrial genes and no open reading frameson JLV5-DEL. Because no genic regions were identified, another deletion, mutation, or rearrangement may condition the MSC phenotype. The association of JLV5-DEL with the MSC phenotype maybe due to separate events occurring in tissue culture which are then transmitted together within the mitochondria.

Last Modified: 10/17/2017
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