Brendan Davies can spot a mutant a mile off. He saw one in his mother's garden the other day, and last year he planted several hundred in his flowerbed. Sadly they haven't reappeared this year.
Dr Davies, from the University of Leeds, studies mutant snapdragons because he is interested in how plants form. Unlike animals, plants have to adapt to life as they are forced to live it and must retain a certain degree of plasticity - grow more or less leaves, flower earlier or later depending on the environmental conditions.
"How is it possible to write an instruction in genes to make something so fantastic," says Davies gesturing towards a snapdragon, "when it takes me more words than it has genes just to describe it?"
According to Professor John Maynard Smith, one of the greatest living evolutionary biologists, this is one of the last unsolved problems in biology: how the seed of a plant, or an egg, turns from a small ball of uniform cells into a sheep, a snake or a snapdragon.
Davies mainly works with Antirrhinum, the common snapdragon, which is flowering at this time of year. The reason he chose the snapdragon stems from one man's obsessive hunt for mutants.
During the early part of this century, a German scientist, Hans Stubbe, subjected snapdragons to radiation, chemicals, X-rays, anything to warp their development. He meticulously categorised and described every possible mutant - and there were many - from plants that form one single flower on the top of their stalk like a sunflower, to double-petalled symmetrical blooms, to sadder specimens that never flower and grow low and close to the ground in tiny rosettes.
Stubbe was trying to find out what makes plants grow? How do they know how to make a leaf, a flower, a seed? As Johann Wolfgang Goethe said: it is only through "our acquaintance with this abnormal metamorphosis, we are enabled to unveil the secrets that normal metamorphosis conceals from us".
"Stubbe was too early," says Davies. "No one could have foreseen the advances we'd make in molecular biology. We look at his mutants and see things that seem obvious now. It wasn't that he wasn't clever, he didn't have the right tools."
After Stubbe's death, the gardeners at the Gatersleben Institute in East Germany looked after his mutants, planting them year after year. Only after the reunification of Germany did the west access this forgotten hoard of plants and information. Davies heard about Stubbe during post-doctoral research in Cologne; on his return to England, he requested seeds from Stubbe's legacy and picked up where he had left off.
Davies has isolated the genes that cause these deformities and worked out which genes do what. One mutant forms tiny cup-shaped leaves. It looks more like a minuscule mushroom than anything floral. This plant has lost the ability to set boundaries. Something has to tell the plant to put forth a leaf and where the edge of the leaf should be. Even if this plant manages to get past the circular leaf stage, it produces fused leaves, and thick masses of swollen, undifferentiated green tissue: a fleshy clump of plant matter.
Davies has recently discovered another gene which causes flowers to form with sterile male parts; he named it Farinelli after the eighteenth century castrato singer.
One of Davies's colleagues, Dr Cathie Martin, from the John Innes Centre in Norwich, worked on a mutant that possibly only the sharp-eyed Stubbe might have noticed. It is identical to all others except in one respect: the colour of the petals is dull. Examining the cells under a scanning electron microscope, she discovered that a conical projection normally seen in the middle of petal cells was missing. This pro jection reflects light, giving petals their characteristic brightness and sheen. Martin has discovered the gene which controls the petal projection and managed to insert it and turn it on in tobacco plant leaves.
Many of the genes Davies has been examining are MADS-box genes which control a number of other genes. There are about 90 MADS-box genes that regulate the genes which control reproductive organs, flowering time, root and seed development and fertility. For instance, two genes are mainly responsible for flower formation; if they mutate, the plant is unable to flower. Cauliflower, like broccoli and romanesco, is really the tip of the plant on the verge of flowering but unable to form flowers and is likely to have been formed by a mutation in one of these two MADS-box genes, probably during the 15th century.
Not all mutants are aesthetically unpleasant or could end up on the table: an old set of primula mutants has been retained since Elizabethan times because of the attrac tiveness of their flowers. Margaret Webster, a student at Leeds, holds the National Register of Anomalous Primulas; some have quaint names such as Jack in the Green and Hose in Hose. Once a year, Professor Phil Gilmartin, one of Davies's colleges and Webster's supervisor, has the task of visiting Naples to collect mutants from one of the larger Italian seed growers who specialise in primula production.
This "mutant" research started off as pure science for the sake of furthering our own understanding, but could have implications for food production. "If we understand how something is built, we can modify it," says Davies. MADS-box genes could be manipulated to control flowering time, root development, or even prevent plants, like lettuce, from flowering at all. We may find gourmet restaurants of the future serving cauliflower-like mutants: the messed up flowers of larkspur, lavender, love-in-the-mist, tossed in olive oil and garnished with full blooms.
