Biomedical subjects

Kim E Hammond-Kosack

Publications and source records attributed to Kim E Hammond-Kosack.

6 recordsLinked to original sources

PubMed2026

The hidden costs of using media to mimic the hosts of Fusarium graminearum: An epigenetic perspectives.

Pathogens dynamically reprogrammed gene expression when transitioning between nonhost and host environments. Epigenetic regulation can provide a rapid and reversible mechanism for this shift. Using published data from Shao et al. (2024) and Zhao et al. (2024), we compare chromatin states in the fungus Fusarium graminearum under in vitro trichothecene mycotoxin (deoxynivalenol) inducing conditions and during wheat spike infection. This revealed striking differences in H3K4me3 and H3K27me3 landscapes with the two datasets showing limited overlap in marked genes and distinct genomic distributions. This indicates that chemically induced cultures only partially replicate the complex signals encountered in planta and emphasise the need for infection-reflective experimental designs to accurately characterise pathogenicity mechanisms.

Fusarium↗

PubMed2006

PHI-base: a new database for pathogen host interactions.

To utilize effectively the growing number of verified genes that mediate an organism's ability to cause disease and/or to trigger host responses, we have developed PHI-base. This is a web-accessible database that currently catalogs 405 experimentally verified pathogenicity, virulence and effector genes from 54 fungal and Oomycete pathogens, of which 176 are from animal pathogens, 227 from plant pathogens and 3 from pathogens with a fungal host. PHI-base is the first on-line resource devoted to the identification and presentation of information on fungal and Oomycete pathogenicity genes and their host interactions. As such, PHI-base is a valuable resource for the discovery of candidate targets in medically and agronomically important fungal and Oomycete pathogens for intervention with synthetic chemistries and natural products. Each entry in PHI-base is curated by domain experts and supported by strong experimental evidence (gene/transcript disruption experiments) as well as literature references in which the experiments are described. Each gene in PHI-base is presented with its nucleotide and deduced amino acid sequence as well as a detailed description of the predicted protein's function during the host infection process. To facilitate data interoperability, we have annotated genes using controlled vocabularies (Gene Ontology terms, Enzyme Commission Numbers and so on), and provide links to other external data sources (e.g. NCBI taxonomy and EMBL). We welcome new data for inclusion in PHI-base, which is freely accessed at www4.rothamsted.bbsrc.ac.uk/phibase/.

Algal Proteins↗

PubMed2006

The pathogen-host interactions database (PHI-base) provides insights into generic and novel themes of pathogenicity.

Fungal and oomycete pathogens of plants and animals are a major global problem. In the last 15 years, many genes required for pathogenesis have been determined for over 50 different species. Other studies have characterized effector genes (previously termed avirulence genes) required to activate host responses. By studying these types of pathogen genes, novel targets for control can be revealed. In this report, we describe the Pathogen-Host Interactions database (PHI-base), which systematically compiles such pathogenicity genes involved in pathogen-host interactions. Here, we focus on the biology that underlies this computational resource: the nature of pathogen-host interactions, the experimental methods that exist for the characterization of such pathogen-host interactions as well as the available computational resources. Based on the data, we review and analyze the specific functions of pathogenicity genes, the host-specific nature of pathogenicity and virulence genes, and the generic mechanisms of effectors that trigger plant responses. We further discuss the utilization of PHI-base for the computational identification of pathogenicity genes through comparative genomics. In this context, the importance of standardizing pathogenicity assays as well as integrating databases to aid comparative genomics is discussed.

Computational Biology↗

PubMed2006

Dominant-negative interference with defence signalling by truncation mutations of the tomato Cf-9 disease resistance gene.

The tomato Cf-9 gene confers resistance to races of the leaf mould fungus Cladosporium fulvum that carry the Avr9 avirulence gene. Cf-9 was isolated by transposon tagging using a modified maize Dissociation (Ds) element. This generated an allelic series of Ds-induced mutations of Cf-9, of which two were found to confer novel phenotypes in a screen for mutants affecting wild-type Cf-9 function in trans. Genetic and molecular analysis of these mutants suggested semidominant, Avr9-dependent, negative-interfering mutations involving Ds insertions in a defined subregion of Cf-9. Interference was associated with expression of the 5'-end of Cf-9 upstream of the Ds insertions in these mutants, suggesting that truncated Cf-9 proteins were the likely cause of interference. Transgenic tomato lines harbouring Cf-9 constructs with premature stop codons in positions similar to the Ds insertions also showed interference, indicating that the presence of Ds was not required for interference to occur. Interestingly, interference in these transgenic lines was completely dominant and was associated with a pronounced developmental phenotype that was dependent on co-expression of Cf-9, Avr9 and a truncated Cf-9 transgene. However, interference with a weakly autoactive Hcr9 gene was Avr9-independent and did not cause a developmental phenotype, suggesting that localized restoration of Cf-9/Avr9-dependent cell death was responsible for the developmental phenotype. The restricted region in which truncation of Cf-9 results in dominant-negative interference suggests that leucine-rich repeats (LRR) 16-19 of Cf-9 may mediate dimerization of Cf-9 and LRRs 20-23 may mediate interactions with downstream partner proteins required for Cf-9 signalling, or vice versa.

Amino Acid Motifs↗

PubMed2003

p-Coumaroylnoradrenaline, a novel plant metabolite implicated in tomato defense against pathogens.

The Avr9 peptide elicitor from the fungus Cladosporium fulvum, the bacterial pathogen Pseudomonas syringae pathovar tomato carrying the avirulence gene avrPto (Pst (avrPto)), and the organophosphorous insecticide fenitrothion induce resistance-related responses in tomato lines carrying the Cf-9, Pto, and Fen genes, respectively. These responses were associated with synthesis of p-coumaroyloctopamine and p-coumaroylnoradrenaline, a novel compound for plants. In susceptible near isogenic tomato lines (Cf-0, pto, fen) and wounded tomato leaves, the levels of these compounds were reduced or undetectable. The elevated levels of p-coumaroyloctopamine and p-coumaroylnoradrenaline were accompanied by elevated mRNA levels of genes encoding phenylalanine ammonia lyase, p-coumarate CoA ligase, and hydroxycinnamoyl-CoA:tyramine N-(hydroxycinnamoyl)transferase (THT), enzymes that are involved in the hydroxycinnamic acid amide biosynthesis. Southern hybridization indicated that THT is encoded by a multigene family in tomato. Four different THT full-length cDNAs were derived by reverse transcriptase-PCR using degenerate primers based on potato and tobacco THT sequences. Transcripts for all four homologs were present in unchallenged tomato leaves, but only tomTHT1-3 was highly expressed following challenge with Pst (avrPto). Furthermore, tomTHT1-3 showed a more substantial and rapid induction in the incompatible interaction than in the compatible interaction. The cDNAs tomTHT1-3, tomTHT7-1, and tomTHT7-8 encoded proteins with a high degree of amino acid sequence homology, although the recombinant proteins had different preferences for octopamine and noradrenaline. The fourth cDNA, tomTHT1-4, directed synthesis of a truncated enzymatically inactive protein due to the presence of a premature stop codon.

Acyltransferases↗

PubMed2003

Deciphering plant-pathogen communication: fresh perspectives for molecular resistance breeding.

Activation of local and systemic plant defences in response to pathogen attack involves dramatic cellular reprogramming. Over the past 10 years many novel genes, proteins and molecules have been discovered as a result of investigating plant-pathogen interactions. Most attempts to harness this knowledge to engineer improved disease resistance in crops have failed. Although gene efficacy in transgenic plants has often been good, commercial exploitation has not been possible because of the detrimental effects on plant growth, development and crop yield. Biotechnology approaches have now shifted emphasis towards marker-assisted breeding and the construction of vectors containing highly regulated transgenes that confer resistance in several distinct ways.

Bacteria↗