Northwest Agriculture and Forestry University published "Cell" articles

Researchers from Virginia Tech, the Northwestern University of Agriculture and Forestry Science and Technology, and the French Academy of Agricultural Sciences have solved the mystery of the pathogenic cause of animal and plant pathogenic oomycetes, which is of great significance for the development of drugs and fungicides. The research results were published in the "Cell" magazine on July 23.

Corresponding authors of the article are Brett M. TylerSee of Virginia Tech and Single Satellite Professor of Northwest A & F University. The latter is currently a professor and doctoral tutor of Northwest A & F University, presiding over the Pathogen-Plant Interaction Laboratory of the School of Biotechnology. Selected as the "New Century Excellent Talent Support Program" by the Ministry of Education in 2005.

According to the Science Times, this study revealed an important breakthrough in the pathogenic mechanism of eukaryotic animal and plant pathogens, especially oomycetes, and found a general mechanism for the entry of eukaryotic pathogen effector proteins into animal and plant host cells.

Oomycetes, including downy mildew, Phytophthora and Pythium, are a class of eukaryotic microorganisms that can cause extensive crop and forestry losses. The potato late blight caused the Irish famine around 1840 and the sudden death of oak trees on the US West Coast around 1990 Disease is the representative. To date, late blight is still the most serious disease problem in potato production. The colonization of pathogens by pathogens and the occurrence of diseases involve a series of small molecule proteins produced by pathogens that exert interference effects in host cells. Although scientists have made breakthroughs in the research of prokaryotic pathogenic bacteria 15 years ago, revealing the key role of the pathogenic bacteria type III secretion system in the transmembrane transport of its effector proteins and entering the host cell, however, it is a transporter for eukaryotic pathogen effector proteins. The understanding of the mechanism is still very limited. How these highly differentiated and diverse eukaryotic pathogen effector proteins enter the host cell and whether there is a common mechanism to enter the host cell is one of the issues of great concern to scientists around the world.

The researchers believe that in the genome of the Phytophthora infestans that has completed the whole genome sequencing, there are 600 to 700 highly differentiated members in the RXLR-like effector protein family alone, and how these effector proteins enter the host cell will contribute to the establishment of new diseases. Prevention and control strategies are of great significance. The research team found that there are a large number of 3-phosphatidylinositol molecules outside the plasma membrane of the plant cell, and the oomycete RXLR effector protein enters the host cell through its binding.

The binding of the RXLR effector protein, which is key to the pathogenicity of oomycetes, to the 3-phosphatidylinositol molecule is mediated by the RXLR domain; the effector protein of plant pathogenic fungi also has a functional domain similar to the oomycete RXLR effector protein, and Binding to the 3-phosphatidylinositol molecule enters the host plant cell.

Professor Shan Weixing has been engaged in the application and basic research of potato late blight prevention and control. During his postdoctoral studies at the University of California, Davis, he identified three non-toxic genes of Phytophthora sojae by map-based cloning (Avr1b-1, Avr1b-2 and Avr1k) physical location and finally isolated the non-toxic gene Avr1b-1. Genetically determined that Avr1b traits are controlled by two independent genes (Avr1b-1 and Avr1b-2); revealed several ways of toxic variation of Phytophthora sojae. Found a genetic variation that exists in Phytophthora sojae and is likely to be unique to oomycetes: gene conversion, that is, some heterozygotes are genetically unstable and mutated to pure at some genetic loci Zygote. The frequency of genetic variation of gene conversion varies greatly among different strains, and the genetic differences between these strains may be controlled by a few genes. Through genetic transformation, a unique way of genetic variation, bacteria can easily recombine between closely linked genes and produce a variety of recombination types. These results may partially explain why Phytophthora infestans is susceptible to mutations to overcome plant disease resistance and resistance to fungicides. These works are the first among oomycetes.

Original summary:

External Lipid PI3P Mediates Entry of Eukaryotic Pathogen Effectors into Plant and Animal Host Cells

Highlights
Oomycete and fungal pathogen effectors bind PI3P via their host cell entry motifs
PI3P is abundant on the surface of plant cells and some human cells
Binding to PI3P is required for host cell entry via lipid raft-mediated endocytosis
Blocking of effector entry by exogenous molecules suggests therapeutic strategies
Summary
Pathogens of plants and animals produce effector proteins that are transferred into the cytoplasm of host cells to suppress host defenses. One type of plant pathogens, oomycetes, produces effector proteins with N-terminal RXLR and dEER motifs that enable entry into host cells. We show here that effectors of another pathogen type, fungi, contain functional variants of the RXLR motif, and that the oomLRcete and fungal RXLR motifs enable binding to the phospholipid, phosphatidylinositol-3-phosphate (PI3P). We find that PI3P is abundant on the outer surface of plant cell plasma membranes and, furthermore, on some animal cells. All effectors could also enter human cells, suggesting that PI3P-mediated effector entry may be very widespread in plant, animal and human pathogenesis. Entry into both plant and animal cells involves lipid raft-mediated endocytosis. Blocking PI3P binding inhibited effector entry, suggesting new therapeutic avenues.

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