Plant-Phytophthora interactions

One aspect of our research is aimed at understanding the mechanism by which P. infestans colonizes its plant hosts.

The approximately 60 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 of the members of the genus, P. infestans is a relatively specialized pathogen, infecting the tubers and above-ground parts of a limited number of hosts. These include potato, tomato, petunia, and a few other solanaceous plants. Why P. infestans can only colonize a few host species is unknown. Does P. infestans produce molecules that plants recognize to induce a defense response? Does P. infestans lack genes necessarily to colonize other plants?

Infected potato tuber

Understanding these issues 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, and 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 for potato and tomato growers worldwide. Costs worldwide due to P. infestans are estimated at $5 billion per year including both lost production and costs for fungicides. Understanding the mechanism of pathogenesis can help lead to control measures for plant diseases caused by oomycetes.

Pathogenesis generally involves asexual growth, and the entire disease cycle can be completed in less than a week in the laboratory. Infection typically begins 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 is considered to reflect plant response or the effect of secondary pathogens rather than the effects of a P. infestans 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).

Several strategies are used to identify genes involved in pathogenesis. One approach involves identifying genes induced during pre-infection stages, such as zoospores, germinated zoospore cysts, and appressoria. A combination of genetic and biochemical tools are then used to test the function of such 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.