Abstract

The gibberellin (GA) biosynthesis mutants lh‐1 and lh‐2 have been used to examine the physiological role of GAs in pea seed development. The LH protein is required for the three‐step oxidation of ent‐kaurene to ent‐kaurenoic acid early in the GA biosynthesis pathway. The allele‐specific interaction of lh‐1 and lh‐2 with chemical inhibitors of these three steps suggests that LH encodes the multi‐functional GA biosynthesis enzyme ent‐kaurene oxidase. Unlike the lh‐2 mutation which reduces seed weight and decreases seed survival by ∼50% compared with wild‐type plants, the lh‐1 allele has a transient effect on embryo and seed growth and only slightly increases seed abortion. These seed phenotypes parallel the effects of the two mutant alleles on GA levels in young seeds. Detailed examination of the growth of lh‐1 seeds reveals homeostatic regulation of GA‐promoted embryo and seed growth. Although GA‐deficient seeds grow more slowly than WT seeds, decreased assimilate availability to the developing seeds is not the primary reason for the altered seed development. Instead, GAs act to promote some process(es) required for embryo and seed growth and only indirectly influence the distribution of assimilates. How GA deficiency causes seed abortion is not known but it may simply be a consequence of reduced seed or embryo growth rate. These results demonstrate that even relatively small changes in the levels of GAs in young seeds can alter seed development and suggest that the available GA‐related mutants may represent only a subset of all possible mutants with reduced GA levels or GA signalling.

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