Differential CaKAN3-CaHSF8 associations underlie distinct immune and heat responses under high temperature and high humidity conditions

Abstract

High temperature and high humidity (HTHH) conditions increase plant susceptibility to a variety of diseases, including bacterial wilt in solanaceous plants. Some solanaceous plant cultivars have evolved mechanisms to activate HTHH-specific immunity to cope with bacterial wilt disease. However, the underlying mechanisms remain poorly understood. Here we find that CaKAN3 and CaHSF8 upregulate and physically interact with each other in nuclei under HTHH conditions without inoculation or early after inoculation with R. solanacearum in pepper. Consequently, CaKAN3 and CaHSF8 synergistically confer immunity against R. solanacearum via activating a subset of NLRs which initiates immune signaling upon perception of unidentified pathogen effectors. Intriguingly, when HTHH conditions are prolonged without pathogen attack or the temperature goes higher, CaHSF8 no longer interacts with CaKAN3. Instead, it directly upregulates a subset of HSP genes thus activating thermotolerance. Our findings highlight mechanisms controlling context-specific activation of high-temperature-specific pepper immunity and thermotolerance mediated by differential CaKAN3-CaHSF8 associations.

Lily LlHSFC2 coordinates with HSFAs to balance heat stress response and improve thermotolerance

“…7a). LCI assay has been widely applied to explore the effect of HS on specific protein interactions (Huang et al ., 2021; Niu et al ., 2022; Yang et al ., 2023). Consistent with a previous report (Huang et al ., 2021), we found that the activity of complete luciferase was slightly inhibited by HS, but quickly recovered after HS released (Fig.…”

CaSTH2 disables CaWRKY40 from activating pepper thermotolerance and immunity against Ralstonia solanacearum via physical interaction

“…It is worth pointing out that our results indicate that CaSTH2 silencing increased both pepper immunity and thermotolerance; however, by previous studies, plant immunity is generally repressed by HTS [ 68 ]. One explanation for this is that, as plant immunity and thermotolerance are two biological processes that are closely related, and a subset of regulatory proteins is shared in these two processes when plant is challenged by two stresses individually, and these shared players might act positively or negatively in the two processes [ 22 , 39 , 41 , 42 , 69 ], so the silencing of these proteins might result in increasing plant immunity and thermotolernace. However, upon the challenge of the two stresses simultaneously, plant immunity may be repressed by HTS.…”

Diversity inhibits foliar fungal diseases in grasslands: Potential mechanisms and temperature dependence

“…Temperature may promote the growth and reproduction of some pathogens (Ayres, 1993;Harvell et al, 2002), but this effect can be offset or even reversed by simultaneous increases in host resistance (Garrett et al, 2006), tolerance (Paseka et al, 2020), immunity (Cavieres et al, 2014), and/or defence (Hu et al, 2022). For example, warming stimulates the expression of plant resistance genes (Yang et al, 2023) and hormone signalling transduction (Samaradivakara et al, 2022) in legumes, thereby reducing disease severity (Yan et al, 2023). Moreover, high temperatures are unfavourable for the growth and reproduction of some pathogens, including rusts (Agrios, 2005), which are among the most common pathogens in China's grasslands.…”