Molecular biology of biotic

and abiotic stresses

Hala Eissa
Resistance genes
 Resistance genes

Ø Induced resistance mechanisms are of major importance in the

defence of plants against pathogens.
Ø Why are these effective in some plants against some pathogens,
but not in others? The answer is complex and presumably
reflects how and when the induction occurs.
Ø In non-host plants, induction of the innate immune response by
non-specific elicitors from microbes may be sufficient for
resistance.
 Resistance genes
Ø In host plants, the pathogen may have evolved to evade these innate
responses or to trigger them later in infection so that they are
ineffective, and specific resistance genes for recognising specific
elicitors from the pathogen may be required for resistance.
Ø These may be either one or a few genes whose individual effects can be
easily detected (gene-for-gene or vertical resistance) or numerous
genes with small additive effects (quantitative or horizontal
resistance).
 Resistance genes

Horizontal versus vertical (gene-for-gene) resistance.

 In horizontal resistance, numerous genes have small additive
effects so that the resistance varies by small amounts between
cultivars.
 In vertical resistance, controlled by single genes, resistance is
either close to complete immunity if the gene is present, or
complete susceptibility if it is absent
 Gene-for-gene resistance
Ø The simple model for how the host resistance mechanism works is through
a dominant resistance (R) gene in the plant encoding a product that
recognises a pathogenicity factor (product of a dominant gene) in the
pathogen to confer resistance.
Ø If the plant does not have this R gene or loses it, it becomes susceptible, or
if the pathogen loses or modifies this pathogenicity gene to avoid
recognition, it will overcome the resistance (although loss of its
pathogenicity factor may also render the pathogen ineffective).
Ø If this occurs, there will be selection pressure on the plant population for
individuals that recognise other pathogenicity factors in the pathogen so
that they can resist it.
Ø Thus an evolutionary ‘arms race’ will develop with complementary changes
occurring in the plant and pathogen populations.
Ø The result in natural plant/pathogen ecosystems would be a balance and
evolutionary stability between plant and pathogen populations.
 Elicitor/receptor model
Ø Recognition of the elicitor derived from the
functional avirulence gene in the
pathogen by the product of the R gene
in the plant activates a signal
transduction pathway leading to the
hypersensitive response and
resistance.
Ø This model has been an important
framework for establishing the
underlying mechanisms of resistance,
although there is increasing evidence
that R genes do not act in isolation from
other genes and pathways in plants,
and that the outcome of any plant-
pathogen interaction is determined by
many genetic factors in both plant and
pathogen.
R gene specificity: Leucine-rich repeats (LRRs)
Ø Leucine-rich repeats (LRRs) are multiple, serial amino
acid repeats (normally around 24 amino acids long)
that contain leucines or other hydrophobic residues at
regular intervals, along with regularly spaced prolines
and asparagines.
Ø Because LRR domains are often involved in protein-
protein interactions in mammalian cells, such as in
hormone receptors that recognise glycoprotein
ligands, or enzyme inhibitors that recognise enzymes,
the identification of these in plant resistance genes
led to the hypothesis that these are the recognition
domains
Ø
R gene specificity: Cellular location of recognition

Ø The receptor-ligand model for R genes initially predicted

that they would encode extracellular receptor-like
proteins to detect the pathogen as it was attempting
ingress into plant cells.
Ø Sequence analysis suggests that some do have LRRs
located extracellularly and tagging experiments have
confirmed the plasma-membrane location for Cf-9.
Ø However, other R-gene products have LRR domains
located within cells. For example, the RPM1 protein for
resistance to P. syringae in Arabidopsis lacks signal
peptides or transmembrane domains and appears to
be linked to the plasma membrane via a second
protein
R gene specificity: Cellular location of recognition
Ø The location of the LRR may also influence the timing of
detection of the invading pathogen, and this in turn may affect
the outcome of the resistance response and account for
some of the variation in degrees of hypersensitive reactions
and pathogen colonisation in different R gene/Avr gene-
dependent interactions.
Ø Resistance responses to the cereal rust fungi, for example,
range from small hypersensitive flecks to medium-sized
uredia pustules surrounded by necrosis depending upon the
resistance gene involved, and this may reflect when the
resistance gene detects the elicitor combined with when the
elicitor is produced by the pathogen.
 Genetic organization of resistance genes
Ø The classical gene-for-gene ‘arms race’ model implies that the
product of a single resistance gene in the plant interacts with
a specific pathogen elicitor.
Ø If the pathogen evolves to lose this elicitor, selection pressure in
the plant will result in another resistance gene capable of
recognising another elicitor.
Ø Evidence from genetics and cloning of R genes indicates that
they are organised in plant genomes in one of two ways:
Ø Simple loci comprising a single gene with minor allelic variation in
gene sequence between plant lines
Ø Genes recognising different avirulence determinants from the same
pathogen are often dispersed throughout the genome