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Beat Keller - One of the best experts on this subject based on the ideXlab platform.
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Host Adaptation through hybridization genome analysis of triticale powdery mildew reveals unique combination of lineage specific effectors
Molecular Plant-microbe Interactions, 2021Co-Authors: Marion C. Müller, Lukas Kunz, Johannes Graf, Seraina Schudel, Beat KellerAbstract:The emergence of new fungal pathogens through hybridization represents a serious challenge for agriculture. Hybridization between the wheat mildew (Blumeria graminis f.sp. tritici) and rye mildew (B.g. f.sp. secalis) pathogens have led to the emergence of a new mildew form (B.g. f.sp. triticale) growing on triticale, a man-made amphiploid crop derived from crossing rye and wheat which was originally resistant to the powdery mildew disease. The identification of the genetic basis of Host-Adaptation in triticale mildew has been hampered by the lack of a reference genome. Here we report the 141.4 Mb reference assembly of triticale mildew isolate THUN-12 derived from long-read sequencing and genetic map-based scaffolding. All eleven triticale mildew chromosomes were assembled from telomere-to-telomere and revealed that 19.7% of the hybrid genome was inherited from the rye mildew parental lineage. We identified lineage-specific regions in the hybrid, inherited from the rye or wheat mildew parental lineages, that harbour numerous bona fide candidate effectors. We propose that the combination of lineage-specific effectors in the hybrid genome is crucial for Host-Adaptation, allowing the fungus to simultaneously circumvent the immune systems contributed by wheat and rye in the triticale crop. In line with this we demonstrate the functional transfer of the SvrPm3 effector from wheat to triticale mildew, a virulence effector that specifically suppresses resistance of the wheat Pm3 allelic series. This transfer is the likely underlying cause for the observed poor effectiveness of several Pm3 alleles against triticale mildew and exemplifies the negative implications of pathogen hybridizations on resistance breeding.
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Host Adaptation through hybridization genome analysis of triticale powdery mildew reveals unique combination of lineage specific effectors
bioRxiv, 2021Co-Authors: Marion C. Müller, Lukas Kunz, Johannes Graf, Seraina Schudel, Beat KellerAbstract:Abstract The emergence of new fungal pathogens through hybridization represents a serious challenge for agriculture. Hybridization between the wheat mildew (Blumeria graminis f.sp. tritici) and rye mildew (B.g. f.sp. secalis) pathogens have led to the emergence of a new mildew form (B.g. f.sp. triticale) growing on triticale, a man-made amphiploid crop derived from crossing rye and wheat which was originally resistant to the powdery mildew disease. The identification of the genetic basis of Host-Adaptation in triticale mildew has been hampered by the lack of a reference genome. Here we report the 141.4 Mb reference assembly of B.g. triticale isolate THUN-12 derived from long-read sequencing and genetic map-based scaffolding. All eleven B.g. triticale chromosomes were assembled from telomere-to-telomere and revealed that 19.7% of the hybrid genome was inherited from the rye mildew parental lineage. We identified lineage-specific regions in the hybrid, inherited from the rye or wheat mildew parental lineages, that harbour numerous bona fide candidate effectors. We propose that the combination of lineage-specific effectors in the hybrid genome is crucial for Host-Adaptation, allowing the fungus to simultaneously circumvent the immune systems contributed by wheat and rye in the triticale crop. In line with this we demonstrate the functional transfer of the SvrPm3 effector from wheat to triticale mildew, a virulence effector that specifically suppresses resistance of the wheat Pm3 allelic series. This transfer is the likely underlying cause for the observed poor effectiveness of several Pm3 alleles against triticale mildew and exemplifies the negative implications of pathogen hybridizations on resistance breeding.
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Non-parent of Origin Expression of Numerous Effector Genes Indicates a Role of Gene Regulation in Host Adaption of the Hybrid Triticale Powdery Mildew Pathogen
Frontiers Media S.A., 2018Co-Authors: Coraline R Praz, Thomas Wicker, Fabrizio Menardo, Salim Bourras, Mark D. Robinson, Marion C. Müller, Beat KellerAbstract:Powdery mildew is an important disease of cereals. It is caused by one species, Blumeria graminis, which is divided into formae speciales each of which is highly specialized to one Host. Recently, a new form capable of growing on triticale (B.g. triticale) has emerged through hybridization between wheat and rye mildews (B.g. tritici and B.g. secalis, respectively). In this work, we used RNA sequencing to study the molecular basis of Host Adaptation in B.g. triticale. We analyzed gene expression in three B.g. tritici isolates, two B.g. secalis isolates and two B.g. triticale isolates and identified a core set of putative effector genes that are highly expressed in all formae speciales. We also found that the genes differentially expressed between isolates of the same form as well as between different formae speciales were enriched in putative effectors. Their coding genes belong to several families including some which contain known members of mildew avirulence (Avr) and suppressor (Svr) genes. Based on these findings we propose that effectors play an important role in Host Adaptation that is mechanistically based on Avr-Resistance gene-Svr interactions. We also found that gene expression in the B.g. triticale hybrid is mostly conserved with the parent-of-origin, but some genes inherited from B.g. tritici showed a B.g. secalis-like expression. Finally, we identified 11 unambiguous cases of putative effector genes with hybrid-specific, non-parent of origin gene expression, and we propose that they are possible determinants of Host specialization in triticale mildew. These data suggest that altered expression of multiple effector genes, in particular Avr and Svr related factors, might play a role in mildew Host Adaptation based on hybridization
Guillaume Sapriel - One of the best experts on this subject based on the ideXlab platform.
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Shared Pathogenomic Patterns Characterize a New Phylotype, Revealing Transition toward Host-Adaptation Long before Speciation of Mycobacterium tuberculosis
Genome Biology and Evolution, 2019Co-Authors: Guillaume SaprielAbstract:Tuberculosis remains one of the deadliest infectious diseases of humanity. To better understand the evolutionary history of Host-Adaptation of tubercle bacilli (MTB), we sought for mycobacterial species that were more closely related to MTB than the previously used comparator species Mycobacterium marinum and Mycobacterium kansasii. Our phylogenomic approach revealed some recently sequenced opportunistic mycobacterial pathogens, Mycobacterium decipiens, Mycobacterium lacus, Mycobacterium riyadhense, and Mycobacterium shinjukuense, to constitute a common clade with MTB, hereafter called MTB-associated phylotype (MTBAP), from which MTB have emerged. Multivariate and clustering analyses of genomic functional content revealed that the MTBAP lineage forms a clearly distinct cluster of species that share common genomic characteristics, such as loss of core genes, shift in dN/dS ratios, and massive expansion of toxin-antitoxin systems. Consistently, analysis of predicted horizontal gene transfer regions suggests that putative functions acquired by MTBAP members were markedly associated with changes in microbial ecology, for example adaption to intracellular stress resistance. Our study thus considerably deepens our view on MTB evolutionary history, unveiling a decisive shift that promoted conversion to Host-Adaptation among ancestral founders of the MTBAP lineage long before Mycobacterium tuberculosis has adapted to the human Host.
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In-Host Adaptation of Salmonella enterica Serotype Dublin during Prosthetic Hip Joint Infection
Emerging Infectious Diseases, 2018Co-Authors: Faten El Sayed, Guillaume Sapriel, Nizar Fawal, Aurelia Gruber, Thomas Bauer, Beate Heym, Caroline Dupont, Henri-jean Garchon, Jean-louis Gaillard, Martin RottmanAbstract:Genome degradation has been central to the Adaptation of Salmonella enterica serotypes to their Hosts throughout evolution. We witnessed the patho-Adaptation of a strain of Salmonella Dublin (a cattle-adapted serotype) to a human Host during the course of a recurrent prosthetic hip joint infection evolving over several years.
Yi Song - One of the best experts on this subject based on the ideXlab platform.
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comparative genome analyses reveal sequence features reflecting distinct modes of Host Adaptation between dicot and monocot powdery mildew
BMC Genomics, 2018Co-Authors: Zhiyong Pan, Shiv D. Kale, Yi Song, Harlan King, Qiong Zhang, Christian Presley, Xiuxin Deng, Cheng-i Wei, Shunyuan XiaoAbstract:Powdery mildew (PM) is one of the most important and widespread plant diseases caused by biotrophic fungi. Notably, while monocot (grass) PM fungi exhibit high-level of Host-specialization, many dicot PM fungi display a broad Host range. To understand such distinct modes of Host-Adaptation, we sequenced the genomes of four dicot PM biotypes belonging to Golovinomyces cichoracearum or Oidium neolycopersici. We compared genomes of the four dicot PM together with those of Blumeria graminis f.sp. hordei (both DH14 and RACE1 isolates), B. graminis f.sp. tritici, and Erysiphe necator infectious on barley, wheat and grapevine, respectively. We found that despite having a similar gene number (6620–6961), the PM genomes vary from 120 to 222 Mb in size. This high-level of genome size variation is indicative of highly differential transposon activities in the PM genomes. While the total number of genes in any given PM genome is only about half of that in the genomes of closely related ascomycete fungi, most (~ 93%) of the ascomycete core genes (ACGs) can be found in the PM genomes. Yet, 186 ACGs were found absent in at least two of the eight PM genomes, of which 35 are missing in some dicot PM biotypes, but present in the three monocot PM genomes, indicating remarkable, independent and perhaps ongoing gene loss in different PM lineages. Consistent with this, we found that only 4192 (3819 singleton) genes are shared by all the eight PM genomes, the remaining genes are lineage- or biotype-specific. Strikingly, whereas the three monocot PM genomes possess up to 661 genes encoding candidate secreted effector proteins (CSEPs) with families containing up to 38 members, all the five dicot PM fungi have only 116–175 genes encoding CSEPs with limited gene amplification. Compared to monocot (grass) PM fungi, dicot PM fungi have a much smaller effectorome. This is consistent with their contrasting modes of Host-adaption: while the monocot PM fungi show a high-level of Host specialization, which may reflect an advanced Host-pathogen arms race, the dicot PM fungi tend to practice polyphagy, which might have lessened selective pressure for escalating an with a particular Host.
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Comparative genome analyses reveal sequence features reflecting distinct modes of Host-Adaptation between dicot and monocot powdery mildew
BMC, 2018Co-Authors: Zhiyong Pan, Shiv D. Kale, Yi Song, Harlan King, Qiong Zhang, Christian Presley, Xiuxin Deng, Cheng-i WeiAbstract:Abstract Background Powdery mildew (PM) is one of the most important and widespread plant diseases caused by biotrophic fungi. Notably, while monocot (grass) PM fungi exhibit high-level of Host-specialization, many dicot PM fungi display a broad Host range. To understand such distinct modes of Host-Adaptation, we sequenced the genomes of four dicot PM biotypes belonging to Golovinomyces cichoracearum or Oidium neolycopersici. Results We compared genomes of the four dicot PM together with those of Blumeria graminis f.sp. hordei (both DH14 and RACE1 isolates), B. graminis f.sp. tritici, and Erysiphe necator infectious on barley, wheat and grapevine, respectively. We found that despite having a similar gene number (6620–6961), the PM genomes vary from 120 to 222 Mb in size. This high-level of genome size variation is indicative of highly differential transposon activities in the PM genomes. While the total number of genes in any given PM genome is only about half of that in the genomes of closely related ascomycete fungi, most (~ 93%) of the ascomycete core genes (ACGs) can be found in the PM genomes. Yet, 186 ACGs were found absent in at least two of the eight PM genomes, of which 35 are missing in some dicot PM biotypes, but present in the three monocot PM genomes, indicating remarkable, independent and perhaps ongoing gene loss in different PM lineages. Consistent with this, we found that only 4192 (3819 singleton) genes are shared by all the eight PM genomes, the remaining genes are lineage- or biotype-specific. Strikingly, whereas the three monocot PM genomes possess up to 661 genes encoding candidate secreted effector proteins (CSEPs) with families containing up to 38 members, all the five dicot PM fungi have only 116–175 genes encoding CSEPs with limited gene amplification. Conclusions Compared to monocot (grass) PM fungi, dicot PM fungi have a much smaller effectorome. This is consistent with their contrasting modes of Host-adaption: while the monocot PM fungi show a high-level of Host specialization, which may reflect an advanced Host-pathogen arms race, the dicot PM fungi tend to practice polyphagy, which might have lessened selective pressure for escalating an with a particular Host
Shunyuan Xiao - One of the best experts on this subject based on the ideXlab platform.
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comparative genome analyses reveal sequence features reflecting distinct modes of Host Adaptation between dicot and monocot powdery mildew
BMC Genomics, 2018Co-Authors: Zhiyong Pan, Shiv D. Kale, Yi Song, Harlan King, Qiong Zhang, Christian Presley, Xiuxin Deng, Cheng-i Wei, Shunyuan XiaoAbstract:Powdery mildew (PM) is one of the most important and widespread plant diseases caused by biotrophic fungi. Notably, while monocot (grass) PM fungi exhibit high-level of Host-specialization, many dicot PM fungi display a broad Host range. To understand such distinct modes of Host-Adaptation, we sequenced the genomes of four dicot PM biotypes belonging to Golovinomyces cichoracearum or Oidium neolycopersici. We compared genomes of the four dicot PM together with those of Blumeria graminis f.sp. hordei (both DH14 and RACE1 isolates), B. graminis f.sp. tritici, and Erysiphe necator infectious on barley, wheat and grapevine, respectively. We found that despite having a similar gene number (6620–6961), the PM genomes vary from 120 to 222 Mb in size. This high-level of genome size variation is indicative of highly differential transposon activities in the PM genomes. While the total number of genes in any given PM genome is only about half of that in the genomes of closely related ascomycete fungi, most (~ 93%) of the ascomycete core genes (ACGs) can be found in the PM genomes. Yet, 186 ACGs were found absent in at least two of the eight PM genomes, of which 35 are missing in some dicot PM biotypes, but present in the three monocot PM genomes, indicating remarkable, independent and perhaps ongoing gene loss in different PM lineages. Consistent with this, we found that only 4192 (3819 singleton) genes are shared by all the eight PM genomes, the remaining genes are lineage- or biotype-specific. Strikingly, whereas the three monocot PM genomes possess up to 661 genes encoding candidate secreted effector proteins (CSEPs) with families containing up to 38 members, all the five dicot PM fungi have only 116–175 genes encoding CSEPs with limited gene amplification. Compared to monocot (grass) PM fungi, dicot PM fungi have a much smaller effectorome. This is consistent with their contrasting modes of Host-adaption: while the monocot PM fungi show a high-level of Host specialization, which may reflect an advanced Host-pathogen arms race, the dicot PM fungi tend to practice polyphagy, which might have lessened selective pressure for escalating an with a particular Host.
Andreas J. Bäumler - One of the best experts on this subject based on the ideXlab platform.
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Pathogenicity Islands and Host Adaptation of Salmonella Serovars
Current topics in microbiology and immunology, 2002Co-Authors: Robert A. Kingsley, Andreas J. BäumlerAbstract:The term ‘pathogenicity island’ was coined in reference to large (70–190kb), unstable genomic regions encoding hemolysin and fimbrial adhesins present in uropathogenic Escherichia coli strains but absent from nonpathogenic isolates, such as the K-12 strain (Blum et al. 1994; Hacker et al. 1983, 1990; Hughes et al. 1987; Knapp et al. 1986; Ritter et al. 1995). The concept helped to explain, in genetic and evolutionary terms, why closely related strains of E. coli may differ substantially in their pathogenic potential. E. coli contains commensal organisms that are part of our normal intestinal flora as well as a number of intestinal and extraintestinal pathogens (Caugant et al. 1983; Nataro and Kaper 1998; Ochman and Selander 1984). In general terms, pathogenicity islands are quintessentially large DNA regions conferring a virulence trait which is absent from a closely related, nonpathogenic, reference species or strain. Analysis of pathogenicity islands in a variety of animal and plant pathogens has revealed a number of common features (Hacker et al. 1997). Pathogenicity islands are often (a) large (> 30kb), (b) inserted in tRNA genes, (c) associated with inverted repeats, transposases, integrases, or plasmid origin of replication, and (d) have a G + C content that is atypical for the pathogen’s genome. In practice, many or none of these may be features of a pathogenicity island.
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identification of a putative salmonella enterica serotype typhimurium Host range factor with homology to ipah and yopm by signature tagged mutagenesis
Infection and Immunity, 1999Co-Authors: Renee M Tsolis, Thomas A Ficht, Garry L Adams, Stacy M Townsend, Edward A Miao, Samuel I Miller, Andreas J. BäumlerAbstract:The genetic basis for the Host Adaptation of Salmonella serotypes is currently unknown. We have explored a new strategy to identify Salmonella enterica serotype Typhimurium (S. typhimurium) genes involved in Host Adaptation, by comparing the virulence of 260 randomly generated signature-tagged mutants during the oral infection of mice and calves. This screen identified four mutants, which were defective for colonization of only one of the two Host species tested. One mutant, which only displayed a colonization defect during the infection of mice, was further characterized. During competitive infection experiments performed with the S. typhimurium wild type, the mutant was defective for colonization of murine Peyer's patches but colonized bovine Peyer's patches at the wild-type level. No difference in virulence between wild type and mutant was observed when calves were infected orally with 1010 CFU/animal. In contrast, the mutant possessed a sixfold increase in 50% lethal morbidity dose when mice were infected orally. The transposon in this mutant was inserted in a 2.9-kb pathogenicity islet, which is located between uvrB and yphK on the S. typhimurium chromosome. This pathogenicity islet contained a single gene, termed slrP, with homology to ipaH of Shigella flexneri and yopM of Yersinia pestis. These data show that comparative screening of signature-tagged mutants in two animal species can be used for scanning the S. typhimurium genome for genes involved in Host Adaptation.
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evolution of Host Adaptation in salmonella enterica
Infection and Immunity, 1998Co-Authors: Andreas J. Bäumler, Renee M Tsolis, Thomas A Ficht, Garry L AdamsAbstract:The question of how bacteria are able to overcome species barriers and adapt to new Hosts is central to the understanding of both the origin of infectious diseases and the emergence of new pathogens. The analysis of virulence factors used by different Salmonella serotypes can serve as a powerful