8. high temperature, A ‘two-edgeD sword’ in crop immunity
In addition to high temperature, plants also have to deal with biotic stresses (e.g. pathogens and pests) along their life cycle (Savary et al., 2019) and those are also affected by a shift in temperature (Bebber, Ramotowski, & Gurr, 2013). Insects propagate more at higher temperature and show increased feeding voracity across an increasing temperature range (Havko et al., 2020). In rice, high temperature contributes to bacterial blight development in field situations, and the disease severity is particularly high in the hot season (Dossa et al., 2020). For more examples related to high temperature-induced disease susceptibility we refer to a recent review (Cohen & Leach, 2020).
While plant defense mechanisms are required to ensure survival and maintain fitness, those usually come at the expense of plant growth, referred to as the “growth-defense tradeoff” (Züst & Agrawal, 2017). As thermomorphogenesis takes place by accelerating growth and development, plant immunity is profoundly affected in Arabidposis(Cheng et al., 2013). For instance, while PHYTOCHROME INTERACTING FACTOR 4 (PIF4), a bHLH transcription factor is stabilized and promotes temperature-mediated growth, it negatively regulates Arabidopsisimmunity (S. Kim et al., 2020; Qiu, Li, Kim, Moore, & Chen, 2019). In addition, plant hormones linked to growth control, such as ABA, brassinosteroids and gibberellic acids, are also involved in plant-immunity pathways. Not rarely, mutants with constitutive activation of defense mechanisms impair growth (Bari & Jones, 2009; D.-L. Yang, Yang, & He, 2013). The accumulation of Heat-shock protein 90 after moderate heat stress correlates to an enhanced wound-induced JA response in tomato. Moreover, JA signaling at high temperature blocked stomata opening and hindered leaf hyponasty, having strong detrimental effects on photosynthesis and inhibiting growth (N. E. Havko et al., 2020).
Two types of high-temperature plant resistance to Pst are known: high-temperature seedling plant (HTSP) resistance and high-temperature adult plant (HTAP) resistance (Chen, 2013). For HTAP resistance toPst in wheat, the kinase-START gene Yr36 (WKS1) (Fu et al., 2009) confers non race-specific resistance to stripe rust, and its expression is upregulated at moderate-high temperatures (25 - 35 °C). However, the resistance conferred by Yr36 is lost at low temperature (e.g. 15°C) and increases plant susceptibility to infections (Fu et al., 2009). In addition, high temperature upregulates the expression of TaXa21 (Wang, Shang, Chen, Xu, & Hu, 2019), a leucine-rich repeat receptor-like kinase gene. The transmembrane and kinase domains of TaXa21 interact with TaWRKY76, which plays a positive role in HTSP resistance to Pst (Wang, H. Shang, et al., 2019; J. Wang et al., 2017). Barley plants also show HTAP resistance to stripe rust, a fungal disease common to wheat and barley (Yan & Chen, 2008).
Bacterial blight caused by Xanthomonas oryzae pv. oryzae(Xoo ) leads to substantial yield loss in rice (Dossa et al., 2020). Xa7, one of the Resistance genes (R -genes) against pathogens (Zhang et al., 2015), effectively confers resistance to Xoo at high temperatures, but not at low temperature (Cohen et al., 2017; Dossa et al., 2020; Webb et al., 2010). The other way around, some biotic stresses mitigate the impairment caused by high temperature stress in crops (Anfoka et al., 2016; Mathur, Sharma, & Jajoo, 2018). However, in the field, different crops are facing different devastating bacterial or fungal diseases with changing temperature, and further molecular mechanisms on low or high temperature-triggered resistance to pathogen diseases are still elusive.