Figure 7: Compromised ETI-mediated restriction of bacterial growth and defense gene activation in arp6–10 and hta9hta11 mutant plants.
From: Plant immune response to pathogens differs with changing temperatures
(a) Bacterial growth assay. Four-week-old plants were hand-inoculated with Pst avrRpm1 or avrRpt2 at 5 × 105cfu ml−1. The bacterial growth was measured 0 days post inoculation (dpi) or 4 dpi. (b) ETI marker gene expression. Four-week-old plants were hand-inoculated with bacteria at 1 × 107cfu ml−1, and RNA was collected 6 hpi for qRT-PCR analysis. The expression of AIG1 and PR1 was normalized to the expression of UBQ10. The data are shown as the mean±s.e.m. (n=3) from three independent biological replicates and the asterisk (*) indicates a significant difference with P<0.05 analysed with the SPSS software one-way ANOVA analysis when compared with data from WT plants. (c) A model of temperature operation of distinct plant innate immune responses. At low ambient temperatures, bacteria secrete a large suite of virulence effectors to promote pathogenicity (ETS), which in turn stimulates plants to co-evolve and preferentially activate ETI signaling. At the elevated temperatures, bacteria multiply vigorously and produce increased amount of MAMPs, which stimulate plants to switch to PTI signaling. Ambient temperature fluctuation likely drives the dynamic co-evolution of bacterial pathogenesis and host immunity. The above experiments were repeated three times with similar results.
