I believe most people have experienced this situation when your fresh, juicy fruits turned into rot

as the time passed. The main reason could be ageing. However, it can be a sign of fungus disease. Botrytis cinerea cause rotten in the fruits and contributes grey mould disease. The other symptoms are soft rots and lesion. Be careful and avoid from eat those fruits because they will harm your health.

wall posses a front shield against fungus, bacteria and virus. It is an effective shield as its pores are much small for microorganism cross over it. Disassemble cell wall is a favorable condition for fungi to infect the plants. In addition, the fungus has some matters that weaken the cell wall.

functions better and causes lesion symptom. In a journal of Pflanzenkr Pflanzenschutz, the scientists revealed that the size of lesion is correlated with the amount of this acid. The production of CWDE is varies and influenced by some factors like the temperature, pH value and host plants. As example, El-Habbaa of Zagazig University, Egypt reported that B. cinerea generate higher galacturonase enzyme at 20oC and 25oC compared to 150C. He also recorded that the fungus isolated from infected, rot strawberry produce less galacturonase enzyme at pH 6.8 than pH 5. In contrast, B. cinerea collected from other host (rot cucumber, rot sweet paper and rose) secretes more enzymes at pH 6.8

death favors the infection process. The fungus continues to develop, infect adjacent cells and increase their population on infected organ. Lucas writes in the Plant Pathology and Plant Pathogens that B. cinerea usually restricted to small lesion. It continues the colonization and form a population with the presence of other closely related species, B. fabae. The population increases over the time till harvest period. Despite the colonization, the plants may detect the fungus and activate their defense system. They can detect it as they sense degraded cell wall that results from CWDE activity. Therefore, fungus colonization might be delayed or avoided. The host plant may counter back by producing diverse defense compounds like antibiotics and antimicrobials. They are vital to neutralize the toxin produced by fungus. The fungus movement or population is restricted with resistance proteins. These proteins trigger hypersensitive response, where the cells surround infection site will death rapidly. Thus, the fungus cannot spread to other part of crops. It remains a hard challenge for farmers and researchers to overwhelm B. cinerea. It infects a broad range of crops and has caused worldwide economic loss around 20% annually, estimated 10-10 billion dollars. The control of this fungus is becoming difficult since it attacks plants close to harvest time and shows no symptom even on harvested crops.

Infection Mechanism
Deteriorate organ that attached to crops or wound part may become an entry route for fungus. Once it land on the plant host, it will break the plant surface. This is completed by enzymes of cutinase and lipase. Upon breaching the plant surface, the fungus extends it pegs and penetrates into a cell wall layer of middle lamella. This layer is rich with a major carbohydrate of pectin. Then, the cell wall layer is degraded by some elements of Cell Wall Degrading Enzyme (CWDE). CWDE consist several enzymes like galacturonase and pectinase. All enzymes cooperate to decrease the thickness and strength of the cell wall. As example, the enzyme galacturonase alone cannot degrade pectin efficiently. But, the other enzyme pectinase will precede the process. Punit Shah at Complex Carbohydrate Research Center, University of Georgia, USA and his colleagues has identified 13 proteins that responsible for pectin degradation in this fungus. The degradation event is assisted by a substance known as oxalic acid. It causes B. cinerea able to do an adjustment onto cell wall environment and creates acidic surrounding. Oxalic acid permits galacturonase

Understanding Botrytis cinerea

B. cinerea is capable to infect over 200 crops. It attacks wide range of fruits including kiwi, apple, pear; vegetables like tomato and cucumber and herbs as well such as sweet pepper. It attacks at several parts/ organs of plant like fruits, flowers, shoot and leaves This fungus travels through air (airborne agent) and spreads by rain and wind. It infects plants prior to harvest, but develops the disease and exhibits the symptoms after post-harvest period. It deposits into the plants and enter quiescent state (stay quietly). It only acts violently when the fruits ripen. So, it is known as an agent of post-harvest disease. In Europe, it is among the main fungi that lead to the post-harvest disease on the table grapes, strawberries and kiwi. Why B. cinerea only attack aggressively towards ripen fruit? During ripening process, the plants gradually mature and soften by altering their structures. The changes take place at cell and molecular level. It includes cell wall disassembling. Cell

The Effects of CWDE

CWDE are important for fungus as a weapon to penetrate the host. It reduces the penetration barrier and eventually accesses the internal tissue. The decomposed cell wall materials in turn become a nutrient source for fungus. There are 2 major consequences when a plant has been invaded by CWDE of B. cinerea. The first one is the fungus may trigger the plant cell death and promotes colonization. The fungus degrades the cell wall, grows within middle lamella and absorbs any sugar, carbohydrate and protein that normally pass through the plant cell. It disrupts host mechanism including defense mechanism and ultimately kills the plant cell. Plant cell

REFERENCES
Publishing El-Habbaa, G.M. (2003) Polygalacturonase Isoenzymes and Cell Wall Degrading Enzymes Secreted by Botrytis cinerea the Causal of Grey Mould Disease on Vegetables. Egypt Journal Phytopathology, 31, 87-101. Germeier, C., Hedke, K. Tiedemann, A.V. (1994) The Use of pH-Indicators in Diagnostic Media for Acid-Producing Plant Pathogens. Pflanzenkr Pflanzenschutz, 85, 82-87. Lucas, J.A. (2002) Plant Pathology and Plant Pathogen, 3rd edition. UK, Blackwell Publishing. ISBN: 9780632030460 Punit, S., Gutierrrez-Sanchez, G. Orlando, R, Bergmann, C. (2009) A Proteomic Study of Pectin Degrading Enzymes Secreted by Botrytis cinerea Grown in Liquid Culture. Proteomics, 9, 3126-3135 Williamson, B., Tudzynski, Tudzynski P., van Kan, J.A.L. (2007) Pathogen Profile, Botrytis cinerea: The Cause of Grey Mould Disease. Molecular Plant Pathology, 8, 561-580.Blackwell

Plant Microbe Interactions C135P1

Title: The Cell Wall Degrading Enzymes of Botrytis cinerea

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