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Supplement bij veertiende jaargang, april 2006 - NVMM

Supplement bij veertiende jaargang, april 2006 - NVMM

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01.01<br />

Innate immunity of plants against fungi; arms race or<br />

balancing selection<br />

P.J.G.M. de Wit, M. Bolton, O. Boras, S. Gabriëls, J. van<br />

’t Klooster, I. Stulemeijer, J. Vossen, P. van Esse. E. Fradin,<br />

U. Ellendorff, I. Stergiopoulos, M. Joosten, B. Thomma.<br />

Wageningen University, Laboratory of Phytopathology,<br />

Wageningen<br />

Avr genes are supposed to have virulence functions in the<br />

absence of the corresponding resistance (R) gene. We have<br />

cloned four Avr and four Ecp genes of the tomato pathogen<br />

Cladosporium fulvum that all encode cysteine-rich peptides<br />

secreted by the fungus during infection of tomato leaves.<br />

Recognition of Avr and Ecp proteins is mediated by Cf<br />

proteins and leads to an innate immune or hypersensitive<br />

response (HR), co-ordinated death of a few host cells at<br />

the site of penetration by the pathogen. C. fulvum avoids<br />

recognition by its host by various mechanisms including:<br />

loss of Avr genes or point mutations, frame shift mutations<br />

or transposon insertions in Avr genes. Avrs are supposed to<br />

interact with a virulence target in the host that is sensed by<br />

Cf proteins that subsequently trigger an HR. Although all<br />

Avr and Ecp proteins are supposed to represent virulence<br />

functions, deletion of single genes do not significantly<br />

reduce virulence of the fungus. For two Avr proteins we<br />

have indications for their biological function. Avr4 is a<br />

chitin-binding protein that protects the fungus against<br />

basic plant chitinases. Avr4 proteins encoded by virulent<br />

alleles in strains of C. fulvum are no longer recognised by<br />

Cf-4 plants, but still bind to chitin, suggesting that chitinbinding<br />

by Avr4 could represent a defensive virulence<br />

function. The Avr2 peptide is secreted by C. fulvum into<br />

the apoplast of tomato leaves and, in the presence of the<br />

tomato extracellular, membrane-anchored Cf2 protein,<br />

triggers the HR that also requires the extracellular tomato<br />

cysteine protease Rcr3. Avr2 binds and inhibits Rcr3, and<br />

the Rcr3-Avr2 complex is subsequently recognized by the<br />

Cf-2 protein.<br />

01.02<br />

Innate immunity of insects<br />

J.M. Reichhart<br />

Strasbourg, France<br />

Drosophila mounts a potent host defence when challenged<br />

by various microorganisms. Molecular and genetic analyses<br />

of this defence have now provided a global picture of<br />

the mechanisms by which this insect senses infection,<br />

discriminates between various classes of microorganisms<br />

A B S T R A C T S<br />

Ned Tijdschr Med Microbiol <strong>2006</strong>; 4:<strong>Supplement</strong><br />

S 5<br />

and induces the production of effector molecules, among<br />

which antimicrobial peptides are prominent. A major<br />

result in these studies was the discovery that most of the<br />

genes involved in the Drosophila host defence are similar<br />

to genes implicated in the mammalian innate immune<br />

response. Recent progress in research on Drosophila<br />

immune defence and the newly discovered similarities or<br />

differences between Drosophila defence mechanisms and<br />

mammalian innate immunity will be discussed.<br />

01.03<br />

Poxvirus immune evasion strategies are linked to host<br />

tropism<br />

G. McFadden<br />

Robarts Research Institute, London, Canada<br />

Despite the eradication of smallpox as an extant human<br />

disease a quarter of a century ago, there remains<br />

considerable fear that variola virus, or other related<br />

pathogenic poxviruses like monkeypox, could emerge<br />

and spread in the human population again. Although<br />

remarkable advances have been made in our understanding<br />

in the molecular events of poxvirus infections, we are still<br />

mostly ignorant about why most poxvirus infections of<br />

vertebrate hosts usually exhibit strict species specificity, or<br />

how zoonotic poxvirus infections occur when poxviruses<br />

occasionally leap into novel host species. Unlike many<br />

other viruses, poxvirus tropism appears to be regulated<br />

not at the level of specific host receptors, but rather at intracellular<br />

events downstream of virus binding and entry.<br />

This seminar summarizes our current understanding of<br />

poxvirus tropism and host range, with specific emphasis on<br />

the prospects for exploiting host-restricted poxvirus vectors<br />

for vaccines or gene therapy and developing host-targeted<br />

oncolytic viral therapies for human cancers. Our lab has<br />

studied one particular poxvirus, myxoma virus, which<br />

exhibits strict species specificity for the rabbit. Targeted<br />

knockout analysis of specific myxoma virus genes has<br />

revealed new clues about the viral and host determinants<br />

of tropism and host range.<br />

01.04<br />

Bacterial innate immune evasion<br />

J.A.G. van Strijp<br />

UMC Utrecht, Eijkman-Winkler Institute, Dept. of Experimental<br />

Microbiology, Utrecht<br />

Upon entering the human body, bacteria are confronted<br />

with the sophisticated innate defense mechanisms of the

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