RNA-seq analysis of hem1 and bi-1a/b/c

Frequent disease outbreaks urge the development of new strategies to enhance plant defense. Tolerance is observed as a successful defense strategy as resistance during virulent pathogen infection. In contrast to resistance, tolerance limits the negative impact of infection on plant health irrespective of pathogen multiplication. However, the genetic and molecular basis remains largely unknown. Here, we discover that alleviating protein condensation at the endoplasmic reticulum (ER) enhances disease tolerance in Arabidopsis. HEM1 and Bax-inhibitor 1 (BI-1), an evolutionary old ER-localized membrane protein, co-condensate during chronic pathogen infection. Their mutual phase separation behaviors facilitate this association and subsequent condensate removal via autophagy. Excessive ER condensates inflict tissue damage, primarily by disrupting lipid homeostasis rather than through unfolded proteins. Moreover, hem1 and bi-1 mutants are defective in co-condensation, exhibit stronger tissue damage resilience, and save plant fitness costs due to virulent bacterial infection. To find out the molecular signature in establishing tolerance, we compared the Psm ES4326-induced transcriptome changes in hem1 or bi-1a/b/c at 24 hpi when no macroscopic disease symptoms developed.