Abstract
Isogenic lines of pea (Pisum sativum L.) were used to determine the physiological site of action of the Rms-2 gene, which maintains apical dominance, and its effect on endogenous free indole-3-acetic acid (IAA) levels. In mutant rms-2 scions, which normally produce lateral branches below node 3 and above node 7, apical dominance was almost fully restored by grafting to Rms-2 (wild-type) stocks. In the reciprocal grafts, rms-2 stocks did not promote branching in wild-type shoots. Together, these results suggest that the Rms-2 gene inhibits branching in the shoot of pea by controlling the synthesis of a translocatable (hormone-like) substance that is produced in the roots and/or cotyledons and in the shoot. At all stages, including the stage at which aerial lateral buds commence outgrowth, the level of IAA in rms-2 shoots was elevated (up to 5-fold) in comparison with that in wild-type shoots. The internode length of rms-2 plants was 40% less than in wild-type plants, and the mutant plants allocated significantly more dry weight to the shoot than to the root in comparison with wild-type plants. Grafting to wild-type stocks did not normalize IAA levels or internode length in rms-2 scions, even though it inhibited branching, suggesting that the involvement of Rms-2 in the control of IAA level and internode length may be confined to processes in the shoot.
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