|Mcgrath, J Mitchell - Mitch|
Submitted to: American Journal of Potato Research
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 9/21/2001
Publication Date: N/A
Interpretive Summary: Potato tuber soft rot can be a devastating post-harvest disease, particular if mechanically damaged, insect infested, or diseased tubers are placed in storage. Pre-emergence loss of rotten seed tubers and post-emergence losses from blackleg stem rot may also be severe at times. This disease is caused by several species of bacteria of the genus Erwinia and only a few potato varieties appear to be resistant or even tolerant to the bacteria. We have found that somatic hybrids of a wild, non-tuber-bearing potato relative, Solanum brevidens are highly resistant to the bacteria. This manuscript describes our effort at analyzing this resistance genetically through 4 generations of crosses. We conclude that a useful level of resistance has been brought into potato by these efforts. As perhaps $200Million in losses of the potato crop can be ascribed to this problem, it is anticipated that incorporation of this resistance into potato cultivars could save millions of dollars in losses in the United States alone.
Technical Abstract: Resistance to potato tuber soft rot caused by Erwinia carotovora was transferred from Solanum brevidens to the cultivated potato over the course of four backcross generations from progeny of a somatic hybrid. Soft rot reactions were determined via a tuber plug inoculation method developed during the course of these experiments. Soft rot resistance was highest in the somatic hybrid (only ca. 20% of tubers and plugs showed evidence of severe rotting) and lowest among progeny of control potato x potato crosses (ca. 80% of tuber plugs showed severe rot). Backcross generations involving somatic hybrids were intermediate in their reaction, and resistance stabilized to about 60% of tuber plugs showing severe rot in the BC2 through the BC4. Reciprocal crosses showed no difference in the inheritance of soft rot resistance, indicating that neither S. brevidens nor S. tuberosum donor cytoplasm had a significant effect on the expression of resistance. Crosses between BC3 siblings where no S. brevidens genetic markers were detected but resistance was segregating demonstrated a dosage effect for soft rot resistance. We conclude that introgression of soft rot resistance has occurred and that at least one of perhaps as few as two loci responsible for resistance in S. brevidens now resides in the S. tuberosum genome.