3.2 Elevated temperature and plant biotic stress interactions
High temperature conditions, along with high humidity, can facilitate
plant disease development by promoting pathogen growth, affecting the
virulence in pathogens, and dampening plant disease resistance responses
(Fujita et al., 2006; Desaint et al., 2020; Zarattini et al., 2021).
High temperature has been shown to increase virulence of pathogens
across diverse plant species (see reviews Cohen & Leach, 2020; Desaint
et al., 2020; Zarattini et al., 2021). For example, resistance of rice
to the fungal pathogen Magnaporthe oryzae is compromised when
plants are pre-exposed to heat stress (Onaga et al., 2017), and barley
(Hordeum vulgare ) is more susceptible to powdery mildew disease
(Blumeria graminis f. sp. hordei ) when exposed to elevated
temperature and CO2 stress (Mikkelsen et al, 2015). This
is also seen in Arabidopsis, where immunity is suppressed in plants
exposed to high temperatures, decreasing resistance of Arabidopsis toP. syringae (Janda et al., 2019). Resistance toXanthomonas in pepper (Capsicum annum ) conferred bybs5, bs6 resistance genes is compromised at elevated temperatures
(Vallejos et al. , 2010). Conversely, pathogen infection has the
potential to compromise heat tolerance, as seen in Tomato yellow
leaf curl virus (TYLCV) in tomatoes (Anfoka et al., 2016).
Virulence in pathogens can also be affected by high temperature stress.
For example, the pathogen responsible for soft rot in potato crops
(Dickeya solani ) causes more severe symptoms in high temperatures
due to an upregulation of genes in D. solani involved in biofilm
production (Czajkowski et al., 2016). Temperature maximums have been
observed however, beyond which pathogen virulence is decreased, as seen
in the phytopathogenic bacterium Pectobacterium carotovorum which
causes bacterial soft rot in a wide range plant species (Saha et al.,
2015). Taken together, there is a complex interaction between
environmental conditions affecting both host plant susceptibility to
pathogen stress and the virulence of the pathogen. For additional review
of heat-dependent plant immune mechanisms and pathogen thermosensory
processes please see Desaint et al., (2020). The authors review
plant-pathogen interactions under elevated temperature stress that have
a negative, neutral, or positive effect on plant resistance,
Work has also been done to identify unique and overlapping responses in
the plant transcriptome to singular and combined temperature and abiotic
stress. A key point of interaction between high temperature and disease
resistance is R protein stability (Fujita et al., 2006; Cohen & Leach,
2020). Previous work has shown that plant resistance is maintained or
enhanced at high temperatures, as seen in expression of several R genes
to wheat stem rust and bacterial blight, however the mechanism for this
enhanced temperature-dependent resistance is not known (Cohen & Leach,
2020). Conversely, disease resistance mediated by receptor-like kinase
(RLK)-type R genes are also compromised by high temperature, indicating
the stability of RLK-type R proteins might also be decreased, weakening
key components of defense signaling in plants (Fujita et al., 2006).
Other common plant transcriptomic responses to combined heat and
pathogen stress include activation of transcription factors, increased
expression of stress responsive genes, and downregulation of
photosynthetic and C metabolism genes (Desaint et al., 2020).
There is also an elaborate crosstalk between elevated temperature stress
and plant hormone signaling. The activation of plant defense to biotic
stress involves regulation of several phytohormone pathways, including
SA, JA, and ethylene (ET) (Zarattini et al., 2021). For example,
previous work has shown defense responses in Arabidopsis to P.
syringae mediated by SA can increase under low temperatures (Li et al.,
2020) but are compromised at elevated temperature (Wang et al., 2009;
Huot et al., 2017; Janda et al., 2019). Resistance was compromised at
elevated temperatures in Arabidopsis due to increased expression of
genes that regulate SA, specifically JA signaling (Huot et al., 2017).
When exposed to low temperature stress, however, SA-ET crosstalk
regulates SA-dependent plant responses (Zarattini et al., 2021). This
indicates there are complex temperature-phytohormone signaling
interactions that lead to novel outcomes based on the treatment and
pathosystem. Future work is needed to understand the synergistic
outcomes from the combined stress, as the transcriptional and
phytohormone response from the combined stress is often unpredictable
and specific to different pathosystems (Cohen & Leach, 2020; Desaint et
al., 2020; Zarattini et al., 2021).