scholarly journals ArabidopsisHIPP27is a host susceptibility gene for the beet cyst nematodeHeterodera schachtii

2018 ◽  
Vol 19 (8) ◽  
pp. 1917-1928 ◽  
Author(s):  
Zoran S. Radakovic ◽  
Muhammad Shahzad Anjam ◽  
Elizabeth Escobar ◽  
Divykriti Chopra ◽  
Javier Cabrera ◽  
...  
Keyword(s):  
Susceptibility Gene ◽  
Host Susceptibility

scholarly journals Septoria nodorum blotch of wheat

2018 ◽  
Author(s):  
Lucky Mehra ◽  
Urmila Adhikari ◽  
Christina Cowger ◽  
Peter S Ojiambo
Keyword(s):  
Plant Pathogens ◽  
Flag Leaf ◽  
Susceptibility Gene ◽  
Gene Interaction ◽  
Kernel Weight ◽  
Control Measures ◽  
Host Susceptibility ◽  
Septoria Nodorum ◽  
Wheat Varieties ◽  
Septoria Nodorum Blotch

Septoria nodorum blotch occurs in wheat-growing areas worldwide, but the disease is more prevalent in areas with warm and moist weather, such as the southeastern United States, parts of Europe, southern Brazil, and Australia. The disease affects both the quantity and quality of yield, and the pathogen is capable of affecting wheat at both seedling and adult stages. Historically, losses up to 50% have been reported, in addition to lower grain quality, although in the U.S., lower levels of loss are typical. The yield losses are highest when flag leaf, F-1 (leaf below flag leaf), and F-2 (leaf below F-1) are infected. The disease is known to reduce thousand-kernel-weight, a yield parameter. The fungus undergoes regular cycles of sexual recombination due to the availability of both mating types, and creates genetic variation in its population, thus enhancing its potential to overcome control measures. The pathosystem is also a model system for necrotrophic plant pathogens. So far, nine necrotrophic effectors and host susceptibility gene interaction have been identified, which have the potential to be used in marker assisted selection for breeding resistant wheat varieties.

scholarly journals Identification and characterization of GLDC as host susceptibility gene to severe influenza

2018 ◽  
Vol 11 (1) ◽  
Author(s):  
Jie Zhou ◽  
Dong Wang ◽  
Bosco Ho‐Yin Wong ◽  
Cun Li ◽  
Vincent Kwok‐Man Poon ◽  
...  
Keyword(s):  
Susceptibility Gene ◽  
Host Susceptibility ◽  
Severe Influenza ◽  
Identification And Characterization

scholarly journals Septoria nodorum blotch of wheat

2018 ◽  
Author(s):  
Lucky Mehra ◽  
Urmila Adhikari ◽  
Christina Cowger ◽  
Peter S Ojiambo
Keyword(s):  
Plant Pathogens ◽  
Flag Leaf ◽  
Susceptibility Gene ◽  
Gene Interaction ◽  
Kernel Weight ◽  
Control Measures ◽  
Host Susceptibility ◽  
Septoria Nodorum ◽  
Wheat Varieties ◽  
Septoria Nodorum Blotch

Septoria nodorum blotch occurs in wheat-growing areas worldwide, but the disease is more prevalent in areas with warm and moist weather, such as the southeastern United States, parts of Europe, southern Brazil, and Australia. The disease affects both the quantity and quality of yield, and the pathogen is capable of affecting wheat at both seedling and adult stages. Historically, losses up to 50% have been reported, in addition to lower grain quality, although in the U.S., lower levels of loss are typical. The yield losses are highest when flag leaf, F-1 (leaf below flag leaf), and F-2 (leaf below F-1) are infected. The disease is known to reduce thousand-kernel-weight, a yield parameter. The fungus undergoes regular cycles of sexual recombination due to the availability of both mating types, and creates genetic variation in its population, thus enhancing its potential to overcome control measures. The pathosystem is also a model system for necrotrophic plant pathogens. So far, nine necrotrophic effectors and host susceptibility gene interaction have been identified, which have the potential to be used in marker assisted selection for breeding resistant wheat varieties.

scholarly journals A Host Susceptibility Gene, DR1, Facilitates Influenza A Virus Replication by Suppressing Host Innate Immunity and Enhancing Viral RNA Replication

2015 ◽  
Vol 89 (7) ◽  
pp. 3671-3682 ◽  
Author(s):  
Shih-Feng Hsu ◽  
Wen-Chi Su ◽  
King-Song Jeng ◽  
Michael M. C. Lai
Keyword(s):  
Influenza A Virus ◽  
Influenza A ◽  
Susceptibility Gene ◽  
Influenza Virus Infection ◽  
Rna Replication ◽  
Viral Rna ◽  
Host Susceptibility ◽  
Viral Rdrp ◽  
Genome Wide ◽  
A Genome

ABSTRACTInfluenza A virus (IAV) depends on cellular factors to complete its replication cycle; thus, investigation of the factors utilized by IAV may facilitate antiviral drug development. To this end, a cellular transcriptional repressor, DR1, was identified from a genome-wide RNA interference (RNAi) screen. Knockdown (KD) of DR1 resulted in reductions of viral RNA and protein production, demonstrating that DR1 acts as a positive host factor in IAV replication. Genome-wide transcriptomic analysis showed that there was a strong induction of interferon-stimulated gene (ISG) expression after prolonged DR1 KD. We found that beta interferon (IFN-β) was induced by DR1 KD, thereby activating the JAK-STAT pathway to turn on ISG expression, which led to a strong inhibition of IAV replication. This result suggests that DR1 in normal cells suppresses IFN induction, probably to prevent undesired cytokine production, but that this suppression may create a milieu that favors IAV replication once cells are infected. Furthermore, biochemical assays of viral RNA replication showed that DR1 KD suppressed viral RNA replication. We also showed that DR1 associated with all three subunits of the viral RNA-dependent RNA polymerase (RdRp) complex, indicating that DR1 may interact with individual components of the viral RdRp complex to enhance viral RNA replication. Thus, DR1 may be considered a novel host susceptibility gene for IAV replication via a dual mechanism, not only suppressing the host defense to indirectly favor IAV replication but also directly facilitating viral RNA replication.IMPORTANCEInvestigations of virus-host interactions involved in influenza A virus (IAV) replication are important for understanding viral pathogenesis and host defenses, which may manipulate influenza virus infection or prevent the emergence of drug resistance caused by a high error rate during viral RNA replication. For this purpose, a cellular transcriptional repressor, DR1, was identified from a genome-wide RNAi screen as a positive regulator in IAV replication. In the current studies, we showed that DR1 suppressed the gene expression of a large set of host innate immunity genes, which indirectly facilitated IAV replication in the event of IAV infection. Besides this scenario, DR1 also directly enhanced the viral RdRp activity, likely through associating with individual components of the viral RdRp complex. Thus, DR1 represents a novel host susceptibility gene for IAV replication via multiple functions, not only suppressing the host defense but also enhancing viral RNA replication. DR1 may be a potential target for drug development against influenza virus infection.

scholarly journals A triple threat: the Parastagonospora nodorum SnTox267 effector exploits three distinct host genetic factors to cause disease in wheat

2021 ◽  
Author(s):  
Jonathan K Richards ◽  
Gayan Kariyawasam, Gayan ◽  
Sudeshi Seneviratne ◽  
Nathan A Wyatt ◽  
Steven S Xu ◽  
...  
Keyword(s):  
Cell Death ◽  
Fungal Pathogen ◽  
Susceptibility Gene ◽  
Susceptibility Genes ◽  
Effector Proteins ◽  
Protein Isoforms ◽  
Host Susceptibility ◽  
Local Selection ◽  
Parastagonospora Nodorum ◽  
Host Pathways

Parastagonospora nodorum is a fungal pathogen of wheat. As a necrotrophic specialist, it deploys a suite of effector proteins that target dominant host susceptibility genes to elicit programmed cell death (PCD). Nine effector-host susceptibility gene interactions have been reported in this pathosystem, presumed to be governed by unique pathogen effectors. This study presents the characterization of the SnTox267 necrotrophic effector that hijacks two separate host pathways to cause necrosis. An association mapping approach identified SnTox267 and the generation of gene-disrupted mutants and gain-of-function transformants confirmed its role in Snn2-, Snn6-, and Snn7-mediated necrosis. The Snn2 and Snn6 host susceptibility genes were complementary, and together they functioned cooperatively to elicit SnTox267-induced necrosis in the same light-dependent PCD pathway. Additionally, we showed that SnTox267 targeted Snn7, resulting in light-independent necrosis. Therefore, SnTox267 co-opts two distinct host pathways to elicit PCD. SnTox267 sequence comparison among a natural population of 197 North American P. nodorum isolates revealed 20 protein isoforms conferring variable levels of virulence, indicating continuing selection pressure on this gene. Protein isoform prevalence among discrete populations indicated that SnTox267 has likely evolved in response to local selection pressures and has diversified more rapidly in the Upper Midwest. Deletion of SnTox267 resulted in the upregulation of the unrelated effector genes SnToxA, SnTox1, and SnTox3, providing evidence for a complex genetic compensation mechanism. These results illustrate a novel evolutionary path by which a necrotrophic fungal pathogen uses a single proteinaceous effector to hijack two host pathways to induce cell death.  

scholarly journals The CAR1 Gene Encoding a Cellular Receptor Specific for Subgroup B and D Avian Leukosis Viruses Maps to the Chickentvb Locus

1998 ◽  
Vol 72 (4) ◽  
pp. 3501-3503 ◽  
Author(s):  
Eugene J. Smith ◽  
Jürgen Brojatsch ◽  
John Naughton ◽  
John A. T. Young
Keyword(s):  
Expressed Sequence Tag ◽  
Receptor Gene ◽  
Susceptibility Gene ◽  
Specific Antigen ◽  
Backcross Progeny ◽  
Host Susceptibility ◽  
Cellular Receptor ◽  
Gene Encoding ◽  
Avian Leukosis Viruses ◽  
Car1 Gene

ABSTRACT Host susceptibility to subgroup B, D, and E avian leukosis viruses (ALV) is determined by specific alleles of the chicken tvblocus. Recently, a chicken gene that encodes a cellular receptor, designated CAR1, specific for subgroups B and D ALV was cloned, and it was proposed that this gene was the s3 allele oftvb (J. Brojatsch, J. Naughton, M. M. Rolls, K. Zingler, and J. A. T. Young, Cell 87:845–855, 1996). We now report that in a backcross derived from an F1 (Jungle Fowl × White Leghorn [WL]) male mated with inbred WL females, the cloned ALV receptor gene cosegregated with two markers linked totvb. The two markers used were atvbs1 -specific antigen recognized by the chicken R2 alloantiserum and restriction fragment length polymorphisms associated with the expressed sequence tag com152e. With all three markers, no crossovers were observed among 52 backcross progeny tested and LOD linkage scores of 15.7 were obtained. These data demonstrate that CAR1 is the subgroup B and D ALV susceptibility gene located at tvbs3.

scholarly journals Arabidopsis HIPP27 is a host susceptibility gene for the beet cyst nematode Heterodera schachtii

2017 ◽  
Author(s):  
Zoran S. Radakovic ◽  
Muhammad Shahzad Anjam ◽  
Elizabeth Escobar ◽  
Divykriti Chopra ◽  
Javier Cabrera ◽  
...  
Keyword(s):  
Susceptibility Gene ◽  
Cyst Nematode ◽  
Nematode Infection ◽  
Host Susceptibility ◽  
Heterodera Schachtii ◽  
Starch Accumulation ◽  
Loss Of Function ◽  
Cyst Nematodes ◽  
Root Cells ◽  
Beet Cyst Nematode

SummarySedentary plant-parasitic cyst nematodes are obligate biotrophs that infect the roots of their host plant. Their parasitism is based on modification of root cells to form a hypermetabolic syncytium from which the nematodes draw their nutrients. The aim of this study was to identify nematode susceptibility genes in Arabidopsis thaliana and to characterize their roles in supporting the parasitism of Heterodera schachtii. By selecting genes that were most strongly upregulated in response to cyst nematode infection, we identified HIPP27 (HEAVY METAL-ASSOCIATED ISOPRENYLATED PLANT PROTEIN 27) as a host susceptibility factor required for beet cyst nematode infection and development. Detailed expression analysis revealed that HIPP27 is a cytoplasmic protein and that HIPP27 is strongly expressed in leaves, young roots and nematode-induced syncytia. Loss-of-function Arabidopsis hipp27 mutants exhibited severely reduced susceptibility to H. schachtii and abnormal starch accumulation in syncytial and peridermal plastids. Our results suggest that HIPP27 is a susceptibility gene in Arabidopsis whose loss-of-function reduces plant susceptibility to cyst nematode infection without increasing susceptibility to other pathogens or negatively affecting plant phenotype.

scholarly journals Septoria nodorum blotch of wheat

2018 ◽  
Author(s):  
Lucky Mehra ◽  
Urmila Adhikari ◽  
Christina Cowger ◽  
Peter S Ojiambo
Keyword(s):  
Plant Pathogens ◽  
Flag Leaf ◽  
Susceptibility Gene ◽  
Gene Interaction ◽  
Kernel Weight ◽  
Control Measures ◽  
Host Susceptibility ◽  
Septoria Nodorum ◽  
Wheat Varieties ◽  
Septoria Nodorum Blotch

Septoria nodorum blotch occurs in wheat-growing areas worldwide, but the disease is more prevalent in areas with warm and moist weather, such as the southeastern United States, parts of Europe, southern Brazil, and Australia. The disease affects both the quantity and quality of yield, and the pathogen is capable of affecting wheat at both seedling and adult stages. Historically, losses up to 50% have been reported, in addition to lower grain quality, although in the U.S., lower levels of loss are typical. The yield losses are highest when flag leaf, F-1 (leaf below flag leaf), and F-2 (leaf below F-1) are infected. The disease is known to reduce thousand-kernel-weight, a yield parameter. The fungus undergoes regular cycles of sexual recombination due to the availability of both mating types, and creates genetic variation in its population, thus enhancing its potential to overcome control measures. The pathosystem is also a model system for necrotrophic plant pathogens. So far, nine necrotrophic effectors and host susceptibility gene interaction have been identified, which have the potential to be used in marker assisted selection for breeding resistant wheat varieties.

scholarly journals Consequences of adaptation of TAL effectors on host susceptibility to Xanthomonas

PLoS Genetics ◽  
2021 ◽  
Vol 17 (1) ◽  
pp. e1009310
Author(s):  
Doron Teper ◽  
Nian Wang
Keyword(s):  
Susceptibility Gene ◽  
Promoter Sequence ◽  
Host Susceptibility ◽  
Successful Implementation ◽  
Transcription Activator ◽  
Promoter Regions ◽  
Tal Effectors ◽  
Disease Symptoms ◽  
Dna Binding Specificity ◽  
S Genes

Transcription activator-like effectors (TALEs) are virulence factors of Xanthomonas that induce the expression of host susceptibility (S) genes by specifically binding to effector binding elements (EBEs) in their promoter regions. The DNA binding specificity of TALEs is dictated by their tandem repeat regions, which are highly variable between different TALEs. Mutation of the EBEs of S genes is being utilized as a key strategy to generate resistant crops against TALE-dependent pathogens. However, TALE adaptations through rearrangement of their repeat regions is a potential obstacle for successful implementation of this strategy. We investigated the consequences of TALE adaptations in the citrus pathogen Xanthomonas citri subsp. citri (Xcc), in which PthA4 is the TALE required for pathogenicity, whereas CsLOB1 is the corresponding susceptibility gene, on host resistance. Seven TALEs, containing two-to-nine mismatching-repeats to the EBEPthA4 that were unable to induce CsLOB1 expression, were introduced into Xcc pthA4:Tn5 and adaptation was simulated by repeated inoculations into and isolations from sweet orange for a duration of 30 cycles. While initially all strains failed to promote disease, symptoms started to appear between 9–28 passages in four TALEs, which originally harbored two-to-five mismatches. Sequence analysis of adapted TALEs identified deletions and mutations within the TALE repeat regions which enhanced putative affinity to the CsLOB1 promoter. Sequence analyses suggest that TALEs adaptations result from recombinations between repeats of the TALEs. Reintroduction of these adapted TALEs into Xcc pthA4:Tn5 restored the ability to induce the expression of CsLOB1, promote disease symptoms and colonize host plants. TALEs harboring seven-to-nine mismatches were unable to adapt to overcome the incompatible interaction. Our study experimentally documented TALE adaptations to incompatible EBE and provided strategic guidance for generation of disease resistant crops against TALE-dependent pathogens.

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