‘OLD BLUSH’ OFFERS SOMETHING NEW
by Darrell g.h. Schramm (schrammd[at]earthlink[dot]net)
No doubt you have heard or read that recurrently blooming roses originated in China. True, ‘Autumn Damask’ and Rosa moschata, not from the Far East, do have both a spring and a fall bloom, but these do not compare to the “everblooming roses” or the repeat bloomers of today. The ancient china roses ‘Old Blush’ and ‘Slater’s Crimson China’ are just two of the significant Chinese roses that introduced recurrent bloom into Western roses. And ‘Old Blush’ is particularly exceptional in its remontancy.
But why, you might well ask, do these China roses bloom repeatedly? What do they have that has been passed on to our modern roses? Why do the once-blooming roses differ genetically? Recent genetic research of the last three years or so has provided us with an answer.
Hikaru Iwata, the Japanese geneticist who was one of three scientists responsible for determining the three parents of damask roses in the year 2000, joined a team of researchers in France headed by Fabrice Foucher at the Institute for Agricultural Research in Angers (INRA) to seek the cause of repeat bloom in roses and strawberries. The team was triumphant in its findings. The discovery of a specific gene as a regulator of flowering created a major achievement in the evolutionary history of horticulture.
The gene for continuous or repeated bloom, discovered in 2010, is part of chromosome 3 in roses. In 2011, Foucher’s team learned that the site of that chromosome “coincides with an important tfl1 gene” that affects the blossoming of a plant, that is, it at least partly suppresses a plant’s ability to flower more than once. However, when the gene mutates, it allows a rose to repeat its bloom. Iwata refers to the gene as ksn, short for Koushin, Japanese for recurrently blooming cultivars.
It was first in ‘Old Blush’ that the team noticed the transposition of the gene. In the middle of the ksn gene, a segment of DNA replicates or inserts a copy of itself into a new position on the chromosome. The mutation of the gene prevents its normal functioning, thus allowing repeat or continuous flowering in a rose. In short, genetic interruption causes the mutation, which in turn causes recurrent blooms.
This discovery was confirmed when the team studied various other remontant roses and their corresponding climbers, as well as a few more. Among those studied were ‘Little White Pet’, ‘Pink Chiffon’, ‘Iceberg’, ‘Wendy Cusson’ and ‘Peace’.
‘Little White Pet’, for instance, grows as a very sh ort repeat-blooming sport of the once-blooming climber ‘Félicité Perpétue’. The different vegetal hormones in ‘Little White Pet’ remain few in number. Earlier British research suggests that these natural hormones seem to inhibit flowering. The fewer the hormones, the more the flowering. It appears, then, that the ksn gene translates its information into a protein that adapts to the hormonal signals and suppresses or inhibits flowering of the plant. For that reason ‘Félicité Perpétue’ blooms but once. On the other hand, when the gene does not function, that is, when it mutates, as in the sport ‘Little White Pet’, the rose blooms continually.
In short, in nearly all wild roses and old garden roses such as gallicas, damasks, albas, or centifolias, the ksn gene functions. In tea and china roses—such as ‘Old Blush’—from which most of our modern roses derive (such as floribundas and hybrid teas), the gene does not function. And so, in the absence of the floral suppressor, an interruption has occurred, and thus we have repeat blooming roses.
“Genetic Code.” Science Daily. Web. 2013. Heitzler, Pascal. “Le Mystère de la Remontance Enfin Dévoilé.” (The Mystery of Remontancy at Last Revealed.)
Rosa Anciennes in France vol 18. Autumn 2012.
Hines, Sandra. “Gardener’s Delight Offers Glimpse Into the Evolution of Flowering Plants.” U. of Washington.Science Daily. Sept. 4. 2012.
Iwata, Hikaru, Fabrice Foucher, et al. “The TFL1 Homologue KSN is a Regulator of Continuous Flowering in Rose and Strawberry.” The Plant Journal vol. 69. Jan. 2012.
Not to be used or reprinted without permission of the author. schrammd[at]earthlink[dot]net