ACTION OF THE PLANT ON
THE VIRUS (TMV)
By growing, virus uses large quantities of nitrogen - N concentration
falls in plant-host tissues - the virus don't develope normally:
relieved of its protein envelope, it is in a latent condition
To explain the influence of the plant on the virus, Grandpa would find it difficult to use the same approach as was used for fusarium. A virus does not develop in an artificial environment. It is an absolute parasite which cannot survive outside the living organism, and he do not see how to explain what happened starting from the tomato/TMV relationship.
He therefore chose a different host: tobacco. A plant which he knew and which seemed particularly appropriate to this type of study. The laboratory director and most of his team were studying the influence of temperature on host/parasite relations between tobacco and this same virus (hence the accidental contamination with TMV of a plant infected with fusariosis).
Tobacco has large lanceolate leaves covered with hairs. If a glass rod is dipped into a suspension of the virus and the epidermis of a leaf is rubbed gently with the rod in question, some of the hairs break, allowing the virus to penetrate the plant. Two different cases are then possible:
- Case n° 1. The virus multiplies gently and steadily. It starts by invading the leaf, then gradually colonises the whole plant, including the roots. Without causing any particular reaction, other than white or yellow patches on the surface of the leaves (which is why this disease is called a mosaic), slower growth and poor quality leaves which lose all commercial value. The plant is said to be sensitive or belonging to a variety sensitive to tobacco mosaic virus.
- Case n° 2. Three days after inoculation, at the places where the virus penetrated, small, brown, necrotic marks develop, about two millimetres in diameter. These marks are surrounded by a yellow halo in which the virus can be detected. However, this virus, relieved of its protein envelope, is in a latent condition, incapable of invading the neighbouring tissues, which remain green and healthy. This takes place at normal temperature, because if the plant is placed in a temperature of 30°C, the inactive virus starts to multiply and now invades the neighbouring tissues. This activity will last as long as the plant is at 30°C. If the plant is returned to a 20° C environment, the colonised tissues undergo necrosis with a yellow halo developing around the edges of the necrotic zones. This halo contains the virus, incapable of invasion etc. This plant is said to be hypersensitive to tobacco mosaic.
What is interesting about this story, is that there are three events taking place here, which normally succeed each other: green leaf, yellow leaf, dead leaf. The virus clearly finds a suitable environment in hypersensitive leaves, so that it multiplies very fast, so fast and so intensively that:
- the colonised tissues, literally emptied of their nitrogen, die of old age and undergo necrosis;
- the neighbouring tissues, also involved, are already so poor in nitrogen that they turn yellow, reveal a state of advanced senescence, explaining why the viral particles which have started to multiply cannot complete their growth. This is our TMV, half constituted and having lost all infectious ability, obliged to wait until an external event (such as an increase in temperature) stimulates the plant rejuvenation. With its compulsory corollary: a resurge in nitrogen metabolism.
Is it really necessary to say that Grandpa collected several tobacco plants which nobody needed, to study their reaction to auxin and gibberellin and compare the N content of plants at 30°C with that of plants left at 20°C?