A scourge of mankind: from ancient times into the genomics era.

摘要

Rust diseases cause major losses in yields of crops of global importance. The first step in successful parasitism by a rust fungus is the 'blind' spore germ tube sensing the surface topography of the plant to feel its way to the stomatal opening for entry into the host. The parasite forms specialized infection structures for delivery of effector proteins into the host cells. Each of the several pathogen effector protein interacts with a specific host protein. The protein complexes function as signalling molecules. In the resistant host plant, the protein complexes activate a defence pathway resulting in a hypersensitive reaction causing death of infected cells and thereby limiting spread of the parasite. In the susceptible host plant, the effector proteins presumably act as transcription factors to subvert metabolic pathways and host physiology. The parasite becomes a powerful sink of host-made carbon compounds. The host plant is starved and injured as the parasite produces countless spores capable of aerial dissemination to new host plants. Due to accumulation of mutations in the genes determining pathogenicity, the parasite frequently evolves into newer races that overcome the effects of rust-resistant genes in crop plants introduced from their wild relatives. A 'race' continues between the plant breeders and the coevolving rust races, requiring newer strategies of controlling the rust disease. These could be anti-adhesion fungicides, preventing the adhesion of pathogen on host surface; or by the modification of the host topography by metabolic engineering, such that germ tubes are misdirected from reaching the stomata.