plant genetics

1. The role and regulation of programmed cell
death in plant–pathogen interactions
BY
M.Noman

2. • Programmed cell death (PCD) is a physiological cell death process
involved in the selective elimination of unwanted cells (Ellis et al.,
1991)
• Multicellular organisms require the ability to eliminate excessive or
damaged cells that are formed both during normal development and in
the interaction of the organism with the environment, e.g. under stress
conditions leading to irreversible cell damage, as well as in infection
with pathogens
• The term apoptosis was coined to describe a succession of
morphological changes—including cell shrinkage, nuclear
condensation, membrane blebbing, and rapid elimination by
phagocytosis.

3. • Animal pathogens often target and suppress programmed cell death
(pcd) pathway components to manipulate their hosts
• In contrast, plant pathogens often activate pcd.
• Programmed cell death (PCD) in plants is a crucial
component of development and defence mechanisms.
• It is crucial for defence responses to restrict the spread of pathogens .
• Host cell death occurs during many, but not all, interactions between
plants and the pathogens that infect them.

4. • In plants, different types of PCD play crucial roles in
vegetative and reproductive development (dPCD), as well
as in the reaction to environmental stresses (ePCD).
• Forms of ePCD result in the sacrifice of cells in response
to abiotic stresses, e.g., temperature or irradiation (Petrov et
al. 2015) or biotic aggressors like pathogens.
• Various dPCD events occur during development or growth
stage.
• Cells must die to form organs with proper functions or
shapes (e.g. leaf shape in some plants), or cells die because
they accomplished their function and/or are no longer
required .

5. Interactions with pathogens
• The invasion of an avirulent pathogen leads to a localized HR,
characterized by rapid collapse of the tissue at the immediate and
surrounding regions of the site of infection, and formation of dry
lesions clearly distinguishable from the surrounding healthy
tissue (Lam, 2004).
• In this way, HR protects plants from potential propagation and
development of the pathogen.
• This localized response is frequently accompanied by the induction of
pathogenesis-related genes, the synthesis of secondary metabolites
with protective functions.

6. • HR induction requires recognition by a special protein of the plant
(the R (resistance) gene product) of the respective
protein of the pathogen (the product of the avr protein is the product
(Avr) gene).
• The R and Avr gene pairs can encode various proteins.
• The product of R gene recognizes the viral protein replicase (which
in this case is the product of the avirulence gene) and triggers HR.
• As a result, at the cost of death of a limited number of cells, the plant
prevents the development of viral infection.

7. • During bacterial or fungal infection, a pathogen is located outside the
plant cell, in the intercellular fluid (apoplast).
• Such pathogens affect plant cells by means of so called “effector”
proteins secreted by pathogens into plant cells.
• For controlling some extracellular pathogens, the vacuolar membrane
can be fused with the plasma membrane, permitting the hydrolytic
enzymes of the vacuole to be released into the extracellular space.
• Membrane fusion is induced by the interaction between the plant R
gene product and the pathogen avirulence factor and ends not only
with neutralization of the pathogen, but also with induction of PCD in
the infected plant cells.

10. Contribution of host cell death to virulent
pathogen replication
• In some host–pathogen interactions, pcd has a clear role in promoting
pathogen growth.
• This is especially true for pathogens that secrete toxins to kill host
cells rapidly, presumably to gain nutrition.
• AAL toxin and related molecules induce pcd.
• Alternaria alternata f. sp. lycopersici lacking the AAL toxin has
severely reduced growth on susceptible plants.
• Likewise, the pathogenicity of Cochliobolus victoriae was correlated
with the secretion of the victorin toxins (Wolpert et al., 2002).

11. • Exogenous application of victorin to susceptible oat plants
causes an apoptotic-like response, including mitochondrial
alterations (Curtis and Wolpert, 2002).
• Interestingly, pathogens that secrete AAL or victorin have a
very narrow host range, only infecting specific hosts.
• For this reason, AAL and victorin are considered to be host-
specific toxins.