Associate Professor of Agricultural Biochemistry
Ph.D. 1974, Purdue University
Office: 356 Jeffords Hall
Research Area: Biorecognition, Plant Biochemistry
Courses Taught: General Biochemistry (AGBI 201); Advanced Biochemistry (AGBI 230); Plant Biochemistry (AGBI 250)
Research in my lab centers around biorecognition, the way one cell communicates with the next at a biochemical level. It is essential for normal plant function that adjacent cells are constantly communicating their condition to their neighbors. This communication takes the form of chemical messages sent from one cell to the next. This communication is particularly important in plant disease. We have studied the interaction between the fungus, Phytophthora infestans, and its host, potato. For the plant to respond to the attack, it must identify its attacker and fight off the attack. The host cells must also talk with adjacent cells to mount a general response to the attacker. In the potato system, the fungus is identified by specific fatty a acids present in the fungus but not in the potato host. All races of the fungus contain these fatty acids and can cause the resistant response in all varieties of the host. However, P. infestans is of interest since it causes the disease late blight of potato. To cause disease the fungus must sabotage the normal resistant response of the host. It does this by producing specific suppressors of the resistance response. Hence, in late blight of potato two specific messages are important in the establishment of the disease 1). The fungus is here and 2.) Shut down the resistant response. This work may play an important part in the control of this devastating disease, the cause of the Irish potato famine, which still results in the loss of an average of 10% of the potato crop every year. The introduction to the US of new fungicide resistant strains of the fungus in the last ten years makes this problem even more acute.
We have also worked on the "beneficial disease" nodulation of legumes by Rhizobia. In this interaction the final result is the establishment of a colony of bacteria within the plant. This colony produces the enzymes necessary to fix nitrogen from the air for the use of the plant. The plant supplies sugars to the bacteria in return for the nitrogen fixed. One of the first signals between the plant and the bacteria is a chemical signal that draws the bacteria to the host through the soil. We have shown that specific molecules given off by the plant's roots attract the appropriate strains of rhizobia. After the accumulation of bacteria near the root, they exchange other chemical signals which allow the progress of infection. Understanding of this important interaction may ultimately allow farmers to produce more and better crops without reliance on artificial fertilizers.
Other work in my lab has involved the attraction of apple maggot flies to their host. Specific bacteria are present on the surface of apple fruit and leaves that are necessary for the development of the eggs in the female apple maggot fly. Specific fatty acids are given off by these bacteria which are attractive to the female fly. These attractive fatty acids may be useful in a control strategy for the apple maggot that does not so heavily rely on pesticide sprays.
Currently, I am looking at the signals in the maple tree involved in controlling how much sugar is in the sap. Some trees are genetically programmed to produce up to five times the normal level of sucrose in the sap. These "sweet" trees require less sap and less energy to produce maple syrup. We are using the polymerase chain reaction to correlate physical characteristics of the DNA of both "sweet" trees and normal trees. These DNA markers may prove useful in a breeding program to produce better quality trees for Vermont's sugarbushes. Characterization of the differences between sweet trees and their normal brethren may also give insight into the signals used in the tree to control the level of sugar in the sap.