Information from well-known stem length mutants, both short and elongated, is discussed in the context of criteria necessary to demonstrate that the level of GA1 controls stem elongation in wild- type plants of the garden pea. Whilst this evidence is compelling, a mutant which over-produces GA1 would afford further insight, particularly into whether GA1 levels are saturating for growth in the wild-type. In this paper we further characterise the first reported garden pea mutant (sln) which possesses elevated levels of GA1. Evidence is presented from studies using this mutant that GA1 is normally limiting for growth over the early internodes in wild-type plants. In the developing seed, the mutant sin is shown to block the metabolism of [13C, 3H]GA29 to [13C, 3H]GA29-catabolite, particularly in the testa. Associated with this there were dramatically elevated GAGA29 levels in the dry seed from sln plants (400 times) compared with seeds from Sln plants. Upon germination, it appears that some of this GAGA20 is converted to GAGA1, which leads to substantial elongation of the early internodes. This hypothesis is supported by the observation that the inhibitor of an early step in GA biosynthesis, paclobutrazol, reduces elongation of sln plants when applied to developing seeds but not when applied at the start of germination. By contrast, prohexadione-calcium (BX-112), which inhibits the step GA20 to GA1, dramatically reduces internode length of sln plants when applied to seeds at the start of germination. Finally, application of GA20 to the dry seed of a wild-type (Sln) line (before sowing) resulted in a phenocopy of the sln mutant.