untitled

haustorial biotrophs but then kill the host tissues and
spread within them as necrotrophs (e.g. P. infestanson
potato and P. sojaeon soybean).

Pathogen recognition: the gene-for-gene
hypothesis

In many cropping systems, large areas of land are
sown with a single crop variety (cultivar) that has
been bred for resistance to all known races of the
pathogen. Selection pressure then operates on the
pathogen to overcome this resistance by mutation.
Since many billions of spores are released by the
major pathogens each year – even in a single field –
there is a strong likelihood of the resistance breaking
down. This is especially true for crops that have been
bred for single major gene resistance(R gene resistance)
as opposed to “field resistance” that is based on the com-
bined activities of several “minor” genes. The eminent
plant pathologist H.H. Flor, working with flax rust
(Melampsora lini) in the 1940s and 1950s, proposed a
simple scheme to explain the relationship between
major gene resistance and the occurrence of disease –
the gene-for-gene hypothesis. Based on extensive
research of the genetics of both the host plant and the
pathogen, he showed that for every gene that confers
resistance(R, a genetically dominanttrait) in flax
plants, there is a complementary gene that confers
avirulence(AVR, again a genetically dominanttrait)
in the pathogen. So, the outcome of a host–pathogen
interaction can be summarized in the following table:

prevent a biotroph from developing. In effect, the R

gene product of the host would be like a receptor,

interacting with the AVR gene product (an elicitor) of

the fungus.

Recent research has provided a deeper understand-

ing of this system, and shown that gene-for-gene rela-

tionships are common across a range of host–parasite

combinations, including interactions of plants with

pathogenic fungi, bacteria, viruses, and nematodes,

and even in some plant–insect interactions. A direct

protein–protein interactiongoverned by R genes and

AVR genes, and leading to the hypersensitive response,

has been demonstrated in two pathosystems: infection

of tomato by Pseudomonas syringae(pathovar syringae)

and infection of rice by Magnaporthe grisea(rice blast

disease). In these cases the interaction probably involves

the recognition of surface-located proteins. However,

a directprotein–protein interaction has not been found

in any other host–pathogen systems to date. Instead,

there is mounting evidence that at least a third (plant)

protein is involved in most gene-for gene interactions,

and this third protein (or further proteins) mediates the

defense response. There are several lines of evidence for

this (reviewed by Luderer & Joosten 2001; Bogdanova

2002). For example, the proteins involved in these

interactions seem to be cytoplasmic proteins, not cell

surface receptors involved directly in pathogen recog-

nition, as was once thought. The cytoplasmic proteins

constitute a family, or families, of related proteins

with similar properties. For example, the “model”

plant Arabidopsis thaliana(which is widely used for

molecular genetic studies) contains a gene that codes

for resistance to two bacterial pathogens. The product

of this gene is similar to the resistance gene products

of several other organisms – a gene from tobacco con-

ferring resistance to a virus, a gene from flax conferring

resistance to flax rust, a gene from tomatoconferring

resistance to the fungus Fulvia fulvum, and a gene

from sugar beet conferring resistance to a nematode.

All these resistance gene products have a region of

leucine-rich repeats, and all have a nucleotide-binding

site that could initiate a signalling cascade leading to

activation of the plant’s defense response.

Online resources

Endophytes in US Horse Pastures (Aphis Info Sheet;

Veterinary Services; April 2000). http://

http://www.aphis.usda.gov/vs/ceah/Equine/eq98endoph.htm

Sudden Oak Death. USDA Forest Service. http://www.invasive.org

General texts

Agrios, G.N. (1998) Plant Pathology, 4th edn. Academic Press,

San Diego.

FUNGI AS PLANT PATHOGENS 307

PATHOGEN

GENOTYPE

AVR avr

or

AVR AVR

avr avr

Disease-

resistant

Susceptible

to disease

Susceptible

to disease

RR or Rr rr

Susceptible

to disease

HOST GENOTYPE

where RR=homozygous resistant, Rr=heterozygous
resistant, rr=homozygous susceptible, AVR AVR=
homozygous avirulent, AVR avr=heterozygous avir-
ulent, avr avr=homozygous virulent. From this table
we can see that resistance occurs onlyin combinations
involving the dominant R allele andthe dominant
AVR allele. The simplest explanation would be that
the protein product of the R gene interacts with
the protein product of the AVRgene, leading to the
hypersensitive response – a rapid cell death that would