General and contact information
Howard Judelson's background
education and interests
learn more about these exciting organisms
The late blight disease
learn more about the problems that P. infestans causes
Ongoing research projects
Other lab members
Opportunities for graduate study in the lab
One aspect of our research is aimed at understanding the mechanism by which oomycetes colonize their plant hosts.
The approximately 100 species of Phytophthora are all destructive pathogens, causing rots of tubers, roots, stems, leaves and fruit of a huge range of agriculturally and ornamentally important plants. Unlike some members of the genus, P. infestans is relatively specialized, infecting tubers and above-ground parts of a limited number of hosts. These include potato, tomato, and petunia. Related oomycete species (Pythium and downy mildews) are also very important pathogens.
Related oomycetes (Pythium and downy mildews) are also very important pathogens.
Infected potato tuber
Understanding how P. infestans and relatives infect plants is important since the economic damage to crops in the United States by Phytophthora species is estimated in the tens of billions of dollars, including the costs of control measures; worldwide, it is many times this figure. Late blight of potato, caused by P. infestans, resulted in the Irish potato famine in the 1800s and continues to be a difficult problem worldwide. Costs due to P. infestans are estimated at $7-17 billion per year, including both lost production and costs for control chemicals. Understanding the mechanism of pathogenesis can help lead to control measures for plant diseases caused by oomycetes.
Infected tomato leaf
With P. infestans, infections typically begin when an asexual sporangium lands on the plant and releases zoospores, which encyst and produce a germ tube. Sporangia can also germinate directly. The germ tubes differentiate appressoria which participate in the penetration of the underlying plant cells. When pre-existing openings are present, as is common on potato tubers, however, appressorial penetration is not required. Once entry into the host occurs, intercellular hyphae and haustoria develop (see below) which form biotrophic feeding relationships with the plant. P. infestans is regarded as a hemibiotroph, since only living tissue is colonized. Late during compatible interactions, host cells can die but this may reflect plant response rather than the direct actions of a P. infestans protein or toxin. Towards the end of the disease cycle, new sporangia form on exposed plant surfaces.
Diagram of haustorial apparatus of P. infestans in potato. ema, extrahaustorial matrix, eme, extrahaustorial membrane; fl, lipid bodies; fp, pathogen plasmamembrane; fw, pathogen cell wall; hd, host golgi; hm, host microbody; hp, host plasmamembrane; ht, host tonoplast; hv, host vacuole; hw, wall apposition; wh, haustorium wall. From Hohl and Stossel, Can J Bot 54, p. 903 (1976).
Haustoria--specialized hyphae that enter plant cells--play an important role in pathogenesis. They appear to be a hub for communication with the plant, and possibly for nutrition. We are studying several haustoria-associated proteins that may be important in pathogenesis.
Haustorial protein tagged with green fluorescent protein (GFP)
Several strategies are used to identify genes involved in pathogenesis. One approach involves studying the expression of genes induced during infection, using RNA-seq or other methods.
Expression analysis of genes encoding enzymes that degrade the plant cell wall during infection
A combination of genetics, cell biology, biochemistry, and bioinformatics is then used to test the function of the genes. This has led, for example, to the identification of a network of genes involved in the formation of appressoria.
Effect of silencing P. infestans gene PiBzp1, which encodes a transcription factor that regulates pathways required for host infection. Shown on the left are wild-type spores which are able to effectively make appressoria (A). Transgenic P. infestans silenced for PiBzp1 expression are shown on the right; these do not form appressoria, due to a defect in the recognition of the host substrate.
Plant infection assay using wild-type (A) and mutant (B) P. infestans. The mutant, which is silenced for a candidate gene important in host colonization, is unable to form spreading lesions.
While much emphasis in plant-pathogen interactions has focused on the role of the pathogen effector in establishing a successful disease interaction, of equal importance is understanding how the pathogen establishes a feeding relationship with the plant. How pathogens adapt to the changing nutrient status of their host, and differences between hosts, is largely unknown. To address this we have examined several metabolic pathways of P. infestans during growth in potato and tomato leaves and potato tubers, andin young and older infections. As shown below, nutrient levels vary substantially in these different interaction states:
We also studied the expression of most enzymes involved in core metabolism. We found that several varied substantially between the different interactions, as shown below for selected genes involved in amino acid metabolism. This indicates the metabolic adaptation of P. infestans to its different hosts.