Disease resistance (R) genes are key components in plant immunity. Here, we show that Arabidopsis (Arabidopsis thaliana) E3 ubiquitin ligase genes HISTONE MONOUBIQUITINATION1 (HUB1) and HUB2 regulate the expression of R genes SUPPRESSOR OF npr1-1, CONSTITUTIVE1 (SNC1) and RESISTANCE TO PERONOSPORA PARASITICA4. An increase of SNC1 expression induces constitutive immune responses in the bonzai1 (bon1) mutant, and the loss of HUB1 or HUB2 function reduces SNC1 upregulation and suppresses the bon1 autoimmune phenotypes. HUB1 and HUB2 mediate histone 2B (H2B) monoubiquitination directly at the SNC1 R gene locus to regulate its expression. In addition, SNC1 and HUB1 transcripts are moderately up-regulated by pathogen infection, and H2B monoubiquitination at SNC1 is enhanced by pathogen infection. Together, this study indicates that H2B monoubiquitination at the R gene locus regulates its expression and that this histone modification at the R gene locus has an impact on immune responses in plants.

A genome-wide-association study of rice natural varieties identifies a stress-associated protein, OsSAP16, as a positive regulator of low-temperature germination in rice.

Calcium signaling has been postulated to be critical for both heat and chilling tolerance in plants, but its molecular mechanisms are not fully understood. Here, we investigated the function of two closely related cyclic nucleotide-gated ion channel (CNGC) proteins, OsCNGC14 and OsCNGC16, in temperature-stress tolerance in rice (Oryza sativa) by examining their loss-of-function mutants generated by genome editing. Under both heat and chilling stress, both the cngc14 and cngc16 mutants displayed reduced survival rates, higher accumulation levels of hydrogen peroxide, and increased cell death. In the cngc16 mutant, the extent to which some genes were induced and repressed in response to heat stress was altered and some Heat Shock factor (HSF) and Heat Shock Protein (HSP) genes were slightly more induced compared to the wild type. Furthermore, the loss of either OsCNGC14 or OsCNGC16 reduced or abolished cytosolic calcium signals induced by either heat or chilling stress. Therefore, OsCNGC14 and OsCNGC16 are required for heat and chilling tolerance and are modulators of calcium signals in response to temperature stress. In addition, loss of their homologs AtCNGC2 and AtCNGC4 in Arabidopsis (Arabidopsis thaliana) also led to compromised tolerance of low temperature. Thus, this study indicates a critical role of CNGC genes in both chilling and heat tolerance in plants, suggesting a potential overlap in calcium signaling in response to high-and low-temperature stress.

Calcium signaling is essential for environmental responses including immune responses. Here, we provide evidence that the evolutionarily conserved protein BONZAI1 (BON1) functions together with autoinhibited calcium ATPase10 (ACA10) and ACA8 to regulate calcium signals in Arabidopsis. BON1 is a plasma membrane localized protein that negatively regulates the expression of immune receptor genes and positively regulates stomatal closure. We found that BON1 interacts with the autoinhibitory domains of ACA10 and ACA8, and the aca10 loss-of-function (LOF) mutants have an autoimmune phenotype similar to that of the bon1 LOF mutants. Genetic evidences indicate that BON1 positively regulates the activities of ACA10 and ACA8. Consistent with this idea, the steady level of calcium concentration is increased in both aca10 and bon1 mutants. Most strikingly, cytosolic calcium oscillation imposed by external calcium treatment was altered in aca10, aca8, and bon1 mutants in guard cells. In addition, calcium-and pathogen-induced stomatal closure was compromised in the aca10 and bon1 mutants. Taken together, this study indicates that ACA10/8 and BON1 physically interact on plasma membrane and function in the generation of cytosol calcium signatures that are critical for stomatal movement and impact plant immunity.