Welcome to Scribd, the world's digital library. Read, publish, and share books and documents. See more
Download
Standard view
Full view
of .
Look up keyword
Like this
10Activity
0 of .
Results for:
No results containing your search query
P. 1
Fungal pathogenicity genes

Fungal pathogenicity genes

Ratings: (0)|Views: 247|Likes:
Published by darshan418

More info:

Categories:Types, Research, Science
Published by: darshan418 on Jun 10, 2009
Copyright:Attribution Non-commercial

Availability:

Read on Scribd mobile: iPhone, iPad and Android.
download as PDF, TXT or read online from Scribd
See more
See less

01/09/2013

pdf

text

original

 
 1 
Fungal pathogenicity genes
Paul Tudzynski
1
and Amir Sharon
2
 
1
Institut für Botanik, Schlossgarten 3, D-48149 Münster, Germany;
 
2
Department of Plant Sciences, Tel Aviv University, Tel Aviv 69978, Israel
Molecular genetic tools in recent years allowed the identification and detailed functionalanalysis of genes involved in the interplay of pathogenic fungi and their host plants. In thefocus of interest today are genes involved in signaling events which accompany and controlall stages in the infection and colonization processes. From the view point of developingchemical control strategies, specially the early events in the interaction (i.e. the surface-boundevents) are of interest. Further milestones are genes controlling the different life styles of fungi (bio-/necrotroph) and genes involved in overcoming/suppressing the host's defense. Inaddition, "black box" approaches based on genomic data have provided sets of new genesobviously involved in the interaction, but where the details of function have yet to be workedout. This chapter represents a candid shot of a rapidly developing field of research.Abbreviations: AOS - active oxygen species; CWDE – cell wall degrading enzymes; MAPK  – mitogen activated protein kinase; PKA – protein kinase A; REMI – restriction enzymemediated integration.
1. INTRODUCTION
The factors influencing the interaction of pathogenic fungi and their hosts have been amajor research topic in the fungal community in recent years. These detailed investigationshave been fuelled by the necessity to develop new strategies for the control of theseeconomically highly important organisms; inspite of strong efforts to develop and introducenew fungicides and resistant plant varieties, losses due to fungal diseases especially inagriculture are a growing stimulus for basic research in this field. An essential cue in thisongoing battle is the search for fungicide targets via the identification of pathogenicitydeterminants, encoded by pathogenicity genes. The definitions of pathogenicity genes aremanifold; we will follow here the definition of Idnurm and Howlett (2001), which described pathogenicity genes "as genes necessary for desease development, but not essential for the pathogen to complete its lifecycle
in vitro
". We are aware of the problem to apply thisdefinition on biotrophic (non-culturable) fungi. We definitely will not deal here with basic"housekeeping" genes (e.g. aminoacid metabolism, etc.), though for practical purposes(definition of targets for fungicides) also basic genes might be of high importance. We willnot differentiate between pathogenicity genes (yes or no) and virulence genes (modulatingdesease severity), because this can for a given gene depend on the host variety, age and typeof tissue involved and on external conditions. And, finally, we will deal mainly with phytopathogens, according to our expertise.We will focus on genes, which have been proved to have impact on pathogenicity, and thisusually involves functional analysis by molecular techniques (disruption or, alternatively,enhanced expression upon contact with host or in infection structure). We will not review theliterature on AVR genes and other fungal mechanisms that suppress disease, although such
 
 2genes may be regarded as pathogenicity factors. The standard approach in the past to identify pathogenicity genes was forward genetics; i.e. indirect evidence for a factor being a pathogenicity determinant (biochemical and/or genetic data) was tested via the isolation anddeletion of the corresponding gene. In parallel, insertional mutagenesis approaches (REMI,transposon tagging, T-DNA) have yielded a wealth of pathogenicity mutants in severalsystems and have led to several new, partly unexpected pathogenicity factors. The genomicsapproaches give additional, seemingly unlimited perspectives (Soanes
et al.
2002);comparative genomic analyses can help to find answers to the old question, what is thedifference between a saprophyte and a parasite. EST-analyses allow the comparison of genesets expressed during pathogenesis and this can help to identify genes common to groups of  pathogens (same host, same organ, etc.). Such comparative studies also can help to overcomeone of the major obstacles of genomic data: the high percentage of ORFs, i.e. putative genesthat show no homology to any annotated gene. ORFs that are present (and timely expressed)in more than one pathogen could be worth to be studied functionally.One major problem for unequivocal identification of pathogenicity determinants isfunction redundancy, which means that the function of a gene could be taken over by others,even if the analysed gene seems to be a single copy one without apparent paralogs in thegenome. Therefore attention has been focused recently on transcription factors and signalchain components that controll whole sets of pathogenicity genes.Important information can also be obtained by comparison of the different life-style of fungi, e.g. the role of homologous genes in biotrophic and necrotrophic fungi (see e.g. theAOS data below), and more important, the differential expression of genes in biotrophic andnecrotrophic phases of the same fungus. The same holds true for the comparative analysis of mutualistic interactions (mycorrhiza, some endophytes), pinpointing the differences and thehomologies to pathogenic systems.In this chapter we will try to present an overview of this rapidly expanding field. We donot intend to provide a complete list of pathogenicity genes, since new genes are addedmonthly. Instead, we will mention some genes in each category, update versus previousreviews, and discuss in some more details genes for which there is more information that candemonstrate general trends. For comprehensive listing of fungal pathogenicity elementsreaders are referred to recent reviews on the subject (Gold
et al.
2001; Oliver and Osbourn1995; Idnurm and Howlett 2001; Tudzynski and Tudzynski 1999, 2001; Yoder and Turgeon,1996; Yoder and Turgeon 2001) as well as to relevant chapters in this volume.
2. SIGNALING
The success of a fungal pathogen depends to a high degree on its ability to perceive and torespond to signals generated by the plant, especially in the very early stages of infection(recognition), but also in later stages involving different cell types/tissues. Despite the rapidlyincreasing number of cloned signal component genes, the initial events of sensing of extracellular signals and transduction into an intracellular signal are still poorly understood.The binding of signal ligands to cell-surface receptors triggers a conformational change of receptors, e.g. in the case of heterotrimeric G proteins by dissociation of the G
α
subunit fromthe ß
 γ
- subunits which activates or inhibits appropriate target effectors such as proteinkinases, adenylate cyclases, phospholipases, and ion channels (Kronstadt 1997). Componentsof signal chains have been studied recently in several pathogenic fungi, focusing on MAPkinase cascades, the classical cAMP pathway (heterotrimeric G-proteins, adenylate cyclase,cAMP-dependent proteinkinase A), and the crosstalk between them. Only in very few model
 
 3systems these investigations have followed up whole signal chains (including receptors anddownstream components), in most cases single components were functionally analysed to pinpoint pathogenicity – related cascades. The data obtained so far allow some generalconclusions:
There are several examples for signal pathways involved only in pathogenicity; i.e.deletions of the corresponding genes do not effect vegetative properties
in vitro
.
Single components (like the different G
α
subunits or MAPK) are highly conserved, evenhighly homologous to mammalian systems.
The components of a given signal chain might differ considerably between fungi.
The same (or highly homologous) components can be members of cascades regulatingdifferent downstream components (see the results of MAPK knockouts in several fungi).In the following a few selected aspects of this field of research, which has developedrapidly into one of the major foci of molecular phytopathology, will be presented.
2.1 Receptors
Fungi undergo specific differentiation and developmental processes in response to distinct physical and chemical environmental signals. All these events start with an initial"recognition phase" in which specific receptors play an important role by detecting surfacecomponents or other ligands and transmitting this information to one or more downstreamsignaling pathways. So far only one fungal gene encoding a pathogenicity-relatedtransmembrane receptor protein,
 PTH11
, was described. It was identified by a REMI-mutagenesis approach in the rice blast fungus
Magnaporthe grisea
(De Zwaan
et al.
1999).The REMI mutant tagged in the
 PTH11
gene was almost fully apathogenic (drastic reductionof appressoria formation). The predicted secondary structure of Pth11p suggested that it is anintegral membrane protein; this was confirmed by
in situ
localization experiments using aPTH11-GFP-gene fusion. Eukaryotic serpentine receptors have typically seventransmembrane domains (Bockaert and Pin 1999), whereas Pth11p appears to have nine,suggesting an atypical structure. Exogenous cAMP suppressed defects associated with
 pth11
mutants, suggesting that Pth11p mediates cellular response through the cAMP pathway.
2.2 Heterotrimeric GTP-binding proteins (G-Proteins)
The importance of heterotrimeric G proteins in regulating diverse processes such asdifferentiation, mating, and pathogenicity has been demonstrated in a number of  phytopathogenic fungi (a recent compilation in Tudzynski and Tudzynski 2001 lists 7species). In most cases two or more G
α
subunit genes were detected, only one of which hadsignificant influence on pathogenicity e.g.,
CPG-1
from the chesnut blight fungus
Cryphonectria parasitica
(Choi
et al.
1995) and
MAGB
from
M. grisea
(Liu and Dean 1997).The defects linked to G
α
knockouts are manifold: e.g., in
ctg-1
mutants of 
Colletotrichumtrifolii
the conidia fail to germinate, demonstrating the requirement of this G
α
- subunit for avery early stage in the life cycle of this pathogen (Truesdell
et al.
2000).
cga1
mutants of thenorthern corn leaf blight fungus
Cochliobolus heterostrophus
show reduced ability to formappressoria on glass surfaces and corn leaves, but nevertheless are able to induce lesions; inaddition, CGA1 appears to be involved in mating: mutants are female sterile (Horwitz
et al.
 1999). In the gray mould fungus
 Botrytis cinerea
,
 
two G
α
genes,
 BCG1
and
 BCG2
, werefunctionally characterized (Tudzynski
et al.
2000). Both genes are expressed
in planta
at veryearly stages of infection. Knock-out-mutants of both genes caused wild type-like primarynecrotic lesions in the first hours of infection on bean and tomato leaves. However, after twodays, no further development was observed for the lesions caused by the
bcg1
mutants,whereas
bcg2
-mutants produced spreading secondary lesions, albeit retarded.

Activity (10)

You've already reviewed this. Edit your review.
1 hundred reads
1 thousand reads
triinv liked this
milana76 liked this
Kuldeep Singh liked this
Kuldeep Singh liked this
rajeevkumar2222 liked this
Gunjanthapa liked this
m_neopane5997 liked this
Sita Hembrom liked this

You're Reading a Free Preview

Download
scribd
/*********** DO NOT ALTER ANYTHING BELOW THIS LINE ! ************/ var s_code=s.t();if(s_code)document.write(s_code)//-->