Tulip breaking virus

''Tulip breaking virus'' is one of five plant viruses of the family ''Potyviridae'' that cause color-breaking of tulip flowers. These viruses infect plants in only two genera of the family Liliaceae: tulips (''Tulipa'') and lilies (''Lilium'').

Also known as the tulip break virus, lily streak virus, lily mosaic virus, or simply TBV, ''Tulip breaking virus'' is most famous for its dramatic effects on the color of the tulip perianth, an effect highly sought after during the 17th-century Dutch "tulip mania".

''Tulip breaking virus'' is a potyvirus. A distant serological relationship between ''Tulip breaking virus'' and tobacco etch virus was discovered in 1971.

''Tulip breaking virus'' (TBV), tulip top-breaking virus (TTBV), tulip bandbreaking virus (TBBV), Rembrandt tulip-breaking virus (ReTBV), and lily mottle virus (LMoV) have all been identified as potyviruses by serology and potyvirus-specific polymerase chain reaction (PCR). In addition, sequence analysis of amplified DNA fragments has classified them all as distinct viruses or strains; recently TTBV has been found to be strain-related to turnip mosaic virus.

Effects of the virus

The virus infects the bulb and causes the cultivar to "break" its lock on a single color, resulting in intricate bars, stripes, streaks, featherings or flame-like effects of different colors on the petals. These symptoms vary depending on the plant variety and age at the time of infection. Different types of colour-breaks depend on the variety of tulip and the strain of the virus. The color variegation is caused either by local fading, or intensification and overaccumulation of pigments in the vacuoles of the upper epidermal layer due to the irregular distribution of anthocyanin; this fluctuation in pigmentation occurs after the normal flower color has developed. Because each outer surface is affected, both sides of the petal often display different patterns.

In the lily species, the virus causes mild to moderate mottling or streaking in the leaves about two weeks after inoculation, and then causes the plant to produce distorted leaves and flowers.

The virus also weakens the bulb and retards the plant's propagation through offset growths; as it progresses through each generation the bulb grows stunted and weak. Eventually it has no strength to flower, and either breaks apart or withers away, ending the genetic line. For this reason the most famous examples of tulips from color-break bulbs – the ''Semper Augustus'' and the ''Viceroy'' – no longer exist.

History

Long thought to be the earliest recorded plant virus, it is now thought that TBV comes second; the earliest reference to a virus-induced leaf chlorosis (possibly tobacco leaf curl virus) was recorded in Japan in 752 AD.

"Breaking" symptomology was first described in 1576 by Carolus Clusius, a Flemish professor of Botany at Leiden, who noted the variegation, or " rectification", so termed because it was believed that with the offset production of an entirely new "broken" bloom the plant was distilling, or rectifying, itself into a pure life form. From p. 513: (The diversity is so very complicated that it is difficult to express in words all its differences. For when whatever seeds of the nascent tulips hat have beencast off and buried by earth eventually sprout, very few f themcompletely retain the mother's original color, but the flowers transform into various colors (however, the largest portion f seedsdeteriorate in the mud). Hence it be that one can see some lowers in part white, in part purple; others, in part red, in part yellow or gold; others, yellow or reddish, white, purple, or red, in which the colors are simultaneously mingled in such a way that, lthougheach of the colors eotherwise separated, they are intermingled, radiating alternately; and hey areeither more intense or more dilute, or mingled together more closely or more sparsely, also sometimes just streaked with the other color; or slightly mingled with the other over the middle of the petal or along the upper edges f the petals)

Clusius's observations continued; in 1585, he was the first to note that "broken" plants also slowly degenerated. "... any tulip thus changing its original colour is usually ruined afterwards and so wanted only to delight its master's eyes with this variety of colours before dying, as if to bid him a last farewell." It was not known that the virus was responsible for this effect, so for centuries breeders believed that it was environmental conditions that attenuated the bulb and caused single colour tulips to break and streak. They tried to induce "rectification" through frequent soil changes (which causing the bulb to go to seed); varying the planting depths so the plant had to struggle in too much or too little soil; applying too much or too little manure; using soil that was either too poor or too rich; or storing the bulbs in exposed conditions so that they would be 'acted' upon by the rain, wind, sun, and extremes of temperature. However, as early as 1637 Dutch growers were able to produce new broken varieties through bulb grafting, by combining "broken" bulbs infected with the virus with healthy bulbs that produced uniformly colored flowers.

At the end of the eighteenth century, the notion that "breaking" in tulips was a manifestation of some kind of chronic disorder or weakness in the bulb was certainly considered among botanists; but it was still more or less believed that adverse environmental conditions were to blame. A comment by William Hanbury in 1770 that: "All variegations are diseases in a plant and nothing is so proper to bring this about as a defect in nutriment." bears out this general attitude. Given the lack of knowledge of human infectious diseases at this time (and well into the 19th century) this was not an unusual conclusion, but what is surprising is that while tulip mosaic disease has a far more impressive and documented history than any other plant virus, the realization that it was a communicable plant disease, let alone a virus, came surprisingly late – a decade after the end of World War I. "Plant virus" to plant pathologists at the time was almost synonymous with the tobacco mosaic virus, which had been discovered in 1897, quite soon after bacteriology had become established as an academic subject. Since the prime characteristics of the tobacco mosaic virus are that it damages the leaves and flowers of the plant, stunts growth, and lowers quantity and quality of the crop, it is puzzling to many academics and scientists that twenty more years passed before "breaking" was even suspected of being virus-induced.

Pathogen discovery

By the mid-1920s, biochemistry was coming into its own, and its impact was felt in virus research. Eventually, it was a series of bulb manipulation experiments begun in 1928 by Dorothy Cayley at the John Innes Horticultural Institution in Merton, South London, England that led to the discovery of the virus. The record of Cayley's experiments are held at the Institution's current location in Norfolk. Caley discovered that by mechanically transferring infected tissue from broken bulbs to healthy bulbs during their dormant state, the virus that caused the break in color would also be transferred. These experiments were further refined down to minute amounts, which led her to correctly conclude that the "virus or enzyme infection" was sap-transmissible, probably transferred by an insect, and the degree of breaking was proportional to the amount of infected tissue introduced.

The virus was eventually proved to be transferred in a non-persistent manner by at least four species of aphids, specifically ''Myzus persicae'' (the most efficient), '' Macrosiphum euphorbiae'', '' Aphis fabae'', and '' Aphis gossypii''. McKenny-Hughes reported in 1934 that '' Dysaphis tulipae'' transmitted the virus between stored tulip bulbs, but this has not been confirmed. The transfer of the virus is non-persistent, which means it is accomplished through the insect feeding. In non-persistent transmission, viruses become attached to the distal tip of the stylet in the insect's mouthparts, so that the next plant it feeds on is inoculated with the virus. The virus does not affect the seed that produces a bulb, only the bulb itself, its leaves and blooms, and its daughter offsets.

It was not until the 1960s that TBV was shown to have flexuous