passages: PMC-2267190-sec-04__text
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passages: Background
  Potato late blight, a disease caused by the oomycete pathogen Phytophthora infestans, is one of the world's most devastating crop diseases. World-wide losses due to late blight exceed several billion dollars annually [1]. Most of the potato cultivars currently grown in the United States are highly susceptible to late blight and control of this disease relies almost exclusively on fungicide applications. The most effective and environmentally sound way for controlling late blight is to incorporate natural resistance into potato cultivars. The pedigrees of many potato cultivars currently used in different countries include late blight resistant germplasm derived from Solanum demissum, Solanum andigena, and other wild species. However, most of the resistance derived from these wild species is controlled by single dominant resistance genes (R genes). These R genes are only effective in preventing the development of late blight if the invading P. infestans race contains the corresponding avirulence genes. This R gene-mediated resistance is often short-lived and is rapidly overcome by new races of the late blight pathogen.
  Solanum bulbocastanum (2n = 2x = 24) is a diploid species that has adapted in the same environment as the late blight pathogen. This wild species was characterized as possessing durable resistance against P. infestans, even under high disease pressure [2,3]. Two resistance genes, RB (Rpi-blb1) and Rpi-blb2, have been cloned from S. bulbocastanum [4-6]. Both genes confer broad-spectrum resistance against a wide range of known P. infestans races. Transgenic potato lines containing a single RB gene showed a high-level resistance in the Toluca Valley, Mexico, where the potato fields are naturally intensively infested with the most diversified P. infestans populations [7]. Most interestingly, transgenic RB plants did not show total immunity to late blight, but instead showed a marked delay in both onset of symptoms and development of lesions. Such rate-limiting resistance may put less selection pressure on the P. infestans populations and protect the durability of this resistance gene. The RB gene therefore provides an excellent model to study the mechanism of broad-spectrum and rate-limiting disease resistances. An understanding of the underlying mechanism of this type of resistance is important for developing strategies to breed durable and sustainable disease resistance.
  Several genes have been implicated in the regulation of R gene function. Of these genes, Rar1 and Sgt1 are among the most extensively studied genes. The Rar1 (required for Mla12 resistance) gene was first identified for its essential role in the function of a subset of Mla genes that confer resistance to barley powdery mildew [8]. The RAR1 protein contains two highly similar but distinct cysteine- and histidine-rich (CHORD) Zn2+-binding domains and was proposed to play a role in stabilizing R proteins in a confirmation that is implicated in receiving pathogen signals [9]. The Sgt1 gene (suppressor of the G2 allele of skp1) is an essential gene with multiple functions in yeast. SGT1 protein was initially identified as a RAR1-interacting partner in a yeast two-hybrid screen [10]. SGT1 may play a role in R protein accumulation [11]. Rar1 and Sgt1 genes are required in various R-gene mediated resistance against viral, bacterial, oomycete or fungal pathogens [12]. However, none of the previously studied R genes showed a race-non-specific and rate-limiting resistance phenotype as the RB gene. In addition, the role the Rar1 and Sgt1 genes are not universal and these genes are not essential for resistance involving some R genes [12,13].
  Besides the two broad-spectrum resistance genes RB and Rpi-blb2, several race-specific late blight resistance genes have also been cloned [14-16]. Numerous late blight resistance genes have recently been mapped in various potato species or populations [17-25]. However, there is almost no information available about the resistance pathways mediated by any of these genes. As an initial effort to understand the RB-mediated late blight resistance pathway, we silenced the Rar1 and Sgt1 genes using an RNAi-based approach in a potato line containing the RB gene. We demonstrated that SGT1, but not RAR1, is essential for the RB-mediated broad-spectrum resistance to potato late blight.
  