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).