Genetics and evolution of leaf development

Genetic regulation of compound leaf morphology

 

 

 

A spontaneous pea mutant was discovered in the glasshouses at the John Innes Centre in the 1960s (Figure 4). The mutant had many defects; flowers without petals and stamens, leaves with too few leaflets and no tendrils. Instead of the normal pinnate leaf architecture of pairs of leaflets and tendrils on a rachis, each mutant leaf had just a single leaflet. The mutation was known as unifoliata. It had been reported once before, when Gösta Eriksson noticed an abnormal type growing in his field trials in Sweden (Eriksson, 1929. Erbkomplexe des Rotklees und der Erbsen. Zeitschrift für Pflanzenzüchtung XIV: 445-475).

 

Both examples of the mutation had been carefully stored in the John Innes Germplasm Collection and it was not until the late 1990s that they were characterised as lesions in a gene encoding the transcription factor LEAFY (Hofer et al., 1997, Current Biology 7: 581-587).

 

 

 

 

It was the similarity between unifoliata flowers, which lack petals and stamens, and the flowers of an Arabidopsis mutant, leafy, which also lack petals and stamens, that enabled us to identify unifoliata. The Arabidopsis LEAFY gene had been cloned (Weigel et al., 1992, Cell 69: 843-859), so it was possible to design oligonucleotide primers based on the Arabidopsis gene sequence, that would amplify the LEAFY gene from pea, by PCR (polymerase chain reaction). We discovered that descendents of Eriksson’s mutant carried a single nucleotide change in their LEAFY gene compared to normal plants. Descendents of the mutant shown in the photograph (Figure 4) had a large deletion in their LEAFY gene – most of the coding sequence was missing. These defective genes encode defective proteins that fail to carry out their normal cellular functions, resulting in the abnormal organ development seen in the unifoliata mutants.

 

In Arabidopsis flowers, the protein encoded by LEAFY normally activates other transcription factors, which in turn orchestrate the genes required for normal development of petals and stamens. This doesn’t happen in the abnormal flowers of leafy mutants, nor presumably, in the abnormal flowers of unifoliata mutants where the pea version (orthologue) of LEAFY is defective.

 

The unifoliata mutants suggested that UNIFOLIATA (= LEAFY) is normally involved in another gene activation cascade in pea leaves, and this process fails because the gene is defective in abnormal unifoliata leaves (Figure 5).

 

 

 

Figure 5.

A mutant unifoliata leaf (left) and a wild-type (normal) pea leaf (right).

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Papers from our lab are highlighted in yellow.

 

 

Norwich Research Park, Colney, Norwich NR4 7UH, UK