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The lh‐2 mutation in garden pea (Pisum sativum L.) blocks an early step in the gibberellin (GA) biosynthesis pathway, the three‐step oxidation of ent‐kaurene to ent‐kaurenoic acid. As a result, only low levels of GAs, including the bioactive GA1, are found in shoots and seeds of lh‐2 plants. Mutant plants are dwarf in stature, and show increased seed abortion and decreased seed weight, compared with seeds of the tall wild‐type (WT) progenitor (cv. Torsdag). The aberrant seed development of lh‐2 plants is associated with reduced levels of GA1 and GA3, and with an accumulation of abscisic acid (ABA) in young seeds (pre‐contact point). This ABA accumulation is typically 3‐ to 4‐fold, and can be up to 6‐fold, compared with control plants. To investigate whether the accumulation of ABA is partly responsible for causing the observed seed abortion in lh‐2 plants, we constructed a double mutant between the lh‐2 allele and wil. The wil mutation blocks ABA biosynthesis, and reduces ABA levels in young seeds by 10‐fold. Introduction of the wil mutation reduces the endogenous ABA levels in young lh‐2 seeds, but fails to rescue the seeds from abortion. This indicates that the effects of lh‐2 on seed development are not mediated through increased ABA levels, and is consistent with previous evidence that GAs are the controlling factor underlying the lh‐2 seed phenotype in pea.
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Batge et al. (1999) studied this question.
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