Article first published online: 28 APR 2006
Volume 100, Issue 3, pages 550–560, July 1997
How to Cite
Ross, J. J., Murfet, I. C. and Reid, J. B. (1997), Gibberellin mutants. Physiologia Plantarum, 100: 550–560. doi: 10.1111/j.1399-3054.1997.tb03060.x
- Issue published online: 28 APR 2006
- Article first published online: 28 APR 2006
- Received 3 April, 1997
Research on gibberellin (GA) mutants is reviewed, focusing on reports, published since 1993. The mutants have usually been identified via a shoot elongation screen. This screen exposes mutations influencing GA synthesis, deactivation and reception, and also those acting further down the elongation pathway. Mutations blocking synthesis lead to a dwarf. GA-responsive phenotype. Numerous such mutations are now known. For some steps homologous mutations are known across 4 to 6 model species. Examples include the early step, geranylgeranyl diphosphate to copalyl diphosphate, and the activation step, GA26to GA1. Several GA-synthesis mutations have now been characterised at the molecular level and all are in structural genes. It is now clear some steps are controlled by gene families with distinct tissue specificity. Further, some enzymes control more than one step in the biosynthetic pathway. The only mutation known to block deactivation. sin in pea, leads to an elongated phenotype.
The GA response mutants are less well understood and are a more diverse group. They include elongated mutants with a constitutive GA response (spy in arabidopsis. la cry-s in pea and sln in barley) or an enhanced GA response (phyB in arabidopsis. lv in pea and Ih in cucumber). Short response mutants include at least three types. One group accumulates GAs and are mostly unresponsive to applied GA (gai in arabidopsis. D8 in maize. Rht3 in wheat). A recently identified group, exemplified by Igr in pea and gas in barley, have a short stature and reduced response but attain full responses with very high doses of exogenous GA. How close these mutations act to GA reception remains to be determined. Lastly, a number of mutants with short stature and reduced GA response differ in overall phenotype from GA-deficient plants and cannot be made to mimic wild type even at high GA application rates. These mutations act beyond GA reception and some have already proved useful in elucidating other pathways that affect shoot elongation. For example, the lk and lkb mutations in pea appear to block brassinolide synthesis and this in turn prevents normal GA-mediated elongation responses.