Submitted to: American Journal of Potato Research
Publication Type: Abstract only
Publication Acceptance Date: 4/1/2007
Publication Date: 2/1/2008
Citation: Bamberg, J.B. 2008. Genetic comparisons of gibberellin mutants in potato [abstract]. American Journal of Potato Research. 85:2. Interpretive Summary:
Technical Abstract: Gibberellin deficient mutants in potato have been published as ga1 (from S. tuberosum ssp. tuberosum and andigena), pito (from the tuberosum cultivar Pito), and ga2 (from the phureja haploid inducing clone “phu-1.22”). We conducted crossing experiments to investigate genetic similarities. When the cultivar Pito was testcrossed with ga1 4x dwarfs, 1/6 of progeny were dwarf, exactly the expectation if Pito is duplex for ga1. Cultivars Pito and known ga1-carriers Superior and Eramosa all have ga1-carrier Early Rose as a common parent, supporting a hypothesis that the mutant described as pito is actually the same allele as ga1 by common descent. When reputed ga2 heterozygous carrier phu-1.22 was ga1 testcrossed, only one of 419 progeny was dwarf, suggesting that ga1 and ga2 are not allelic. We then attempted to create mutant ga2 in homozygous form. Since phu-1.22 does not self, it was outcrossed to individuals from S. bukasovii and S. microdontum populations devoid of dwarfs, then backcrossed to phu-1.22. No dwarfs were found in over 30,000 BC progeny of 44 different F1 hybrids. This suggests that the ga2 mutant may be present only in a particular clonal sport of phu-1.22 in which it was reported, and not in the original phu-1.22 clone tested at the US Potato Genebank. Like pito, ga2 may actually be identical or allelic to ga1, since mutation from the normal to ga1 dwarf allele in phu-1.22 pollen was evident in the single dwarf recovered in the ga1 testcross progeny of phu-1.22. Some special genetic mechanism for relatively frequent mutation at this locus must be present (transposons?), since normal shoots that occasionally arise on dwarf plants show that the recessive ga1 can also spontaneously revert to the dominant functional allele.