Potato century and is responsible for the Irish

Potato
suffers many diseases, among which late blight, the most harmful potato
disease, which is caused by the oomycete pathogen, Phytophthora infestans
(P. infestans) is the causal agent of potato (Solanum
tuberosum) and tomato (S. lycopersicum) late blight. Late blight is
one of the harmful diseases of potato since 19th century and is
responsible for the Irish potato famine in 1845 and still cause damage to the potato
and tomato production (Song, J, et al. 2003). Potato crop in the field and
storage can totally destroy the yield Under favorable climatic conditions for
the pathogen. The
ability of the pathogen in sexual and asexual reproduction can increase its
pathogenicity potential. Clonal reproduction is commonly observed in North
America, South America, Asia, Africa, and parts of Europe (Fry, William E., et al.2008).
Sexual reproduction of this organism was believed that exist only in
Scandinavia and the Toluca Valley in Mexico, but evidence shows the sexual
reproduction take place in other parts of the world include the United States
and Canada as well (Peters,
R.D., et al. 2014). The effector proteins produced by P. infestans
to recognize or attack host plants have a large diversity due to genome
plasticity and develops the pathogen population (Shukla, and B. P. Singh 2017). The pathogen grows
in the host by developing coenocytic mycelium which later produce
sporangiphores that bear sporangia. The development of sporangia followed by
mycelial growth on the leaf, stem, and fruit tissues occurs at temperatures
above 15°C. On the other hand, at the lower temperatures, sporangia forgo
mycelia is developed by forming and releasing zoospores (asexual spores), which
have the ability to grow faster and produce new infections (Nowicky and Majid 2017).
The regeneration time depends on the environmental conditions and takes from 5
to 7 days (Nowicky and
Majid 2017).

 

3. Plant-pathogen
interaction

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3.1
Qualitative resistance

In
contrast to mammals that have an adaptive immunity, plants have an innate
immune system with the ability to sending systematic signals from infected
sites. Pathogen produces small molecules called elicitors or
pathogen/microbe-associated molecular patterns (PAMP/MAMP), that can induce
plant immune response (Jones
and Jeffery 2006). Elicitors include peptides, metabolites, cell wall
components, enzymes, and toxins. Elicitors are recognized by Pattern
recognition receptors (PRRs) which are located in plasma membrane. In response
to foreign molecule attack, the injured host start producing damage-associated
molecular patterns (DAMP), including plant signal molecules. The first line of
plant defense response is through PAMP/pattern-triggered immunity (PTI) or
non-host resistance. PTI activates downstream genes involving in no symptoms or
race-non-specific hypersensitive response (Malinovsky, et al. 2014). Specialized plant
pathogens have specific avirulence (AVR) genes that code race-specific
intracellular elicitors termed effectors, such as (AVR)3a, AVR3b, AVR4, and
AVRSmira1 RXLR effectors, which are secreted into the host cytoplasm, following
penetration of the host cell wall (not membrane) by the pathogen and production
of haustoria to absorb food (Rietman,
H, et al. 2012). Host resistance genes and other PAMPs are suppressed
through effector activity. As a second line of defense response, the effectors
are detected by the host cell membrane receptor proteins (ERR). The R genes code for membrane receptor proteins
with intracellular signaling ability. This detection leads to activation of
plant transcription factors (WRKY, MYB, NAC, and ERF) by transferring signals
through cytosolic protein kinases such as MAPKKK pathway which regulate several
R genes to generate resistance
related protein and metabolites. As a result, a race-specific hypersensitive
response (HR) or death of the infected cells referred to as the effector-
triggered immunity (ETI), qualitative resistance, or vertical resistance
occurred (Yogendra, and
Ajjamada 2016). Plants recognize these elicitors/effectors and mount an
immune response, by triggering a hierarchy of R genes (elicitor recognition
receptor (ELRR), effector recognition receptor (ERR), phytohormone (PHR),
mitogen-activated protein kinase (MAPK), transcription factor (TF)), eventually
to produce resistance-related (RR) metabolites (RRMs) and proteins (RRPs), that
directly suppress the pathogen advancement. The genes like NADPH and Callose
synthase play a role in hypersensitive response significantly, but the effector
recognition receptor genes are just surveillance genes (Pushpa, et al. 2013). Recent studies
demonstrated the role of plant hormone-mediated defense pathways, calcium ions,
and reactive oxygen species (ROS) in activating downstream genes and subsequently
in hypersensitive response or reduced susceptibility (Yogendra, and Ajjamada 2016).