Poison digs its own grave

December 16, 2004

Botrytis cinerea (grey mould) has a large arsenal of molecular pumps at its disposal to protect it against toxic substances such as antibiotics, plant defence compounds and fungicides. Dutch researcher Henk-jan Schoonbeek saw how the fungus started to pump out certain toxic substances within just 15 minutes.

Botrytis cinerea causes rot in fruit and vegetables and is therefore a major problem for growers in horticulture and viniculture. Unfortunately, it is scarcely affected by natural or synthetic protective compounds, as it uses minute protein pumps (so-called ABC transporters) to pump these back out again.

When the fungus comes into contact with toxic substances, these initially enter it unhindered. About 15 minutes later, an emergency mechanism starts up and the fungus secretes the toxic substances so that their concentration in the fungus falls below the lethal dose.

Schoonbeek studied the genes involved in the secretion of toxic substances by ABC transporters. He discovered that the activity of the pumps was partly controlled by the toxic substances. Upon entering the fungus, these stimulate the fungal DNA to produce certain proteins, which then immediately pump these substances out of the fungus.

The researcher established that this mechanism in B. cinerea is comparable to multiple drug resistance in humans. Multiple drug resistance is when cells that have been treated with one type of medicine, become resistant to a completely unrelated group of medicines. Transport proteins also play an important role in multiple drug resistance.

One of these ABC transporters is the protein BcatrB. This protein is involved in defending the fungus against many different toxic substances. For example, it is active against resveratrol, a plant defence compound from grapevines. Therefore the fungus can easily break through the defence lines of grape plants. Although antibiotic-producing bacteria are used to protect plants successfully against other pathogens, the phenazine antibiotics they contain cannot stop B. cinerea. This is because they also activate the production of the BcatrB protein and are therefore immediately pumped back out again. This new information is helpful in developing new strategies to control grey mould diseases.
-end-
The research was funded by the Netherlands Organisation for Scientific Research.

Further information:

Dr Henk-jan Schoonbeek (Wageningen University and Research Centre, now at the University of Fribourg, Switzerland)
t: 41-26-300-8845, henk-jan.schoonbeek@unifr.ch
The doctoral thesis was defended on 29 November 2004, assistant supervisor: Dr M.A. De Waard, supervisor: Prof P.J.G.M. de Wit

Netherlands Organization for Scientific Research

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