CaREM1.4 interacts with CaRIN4 to regulate Ralstonia solanacearum tolerance by triggering cell death in pepper.

Remorins, plant-specific proteins, have a significant role in conferring on plants the ability to adapt to adverse environments. However, the precise function of remorins in resistance to biological stress remains largely unknown. Eighteen CaREM genes were identified in pepper genome sequences based on the C-terminal conserved domain that is specific to remorin proteins in this research. Phylogenetic relations, chromosomal localization, motif, gene structures, and promoter regions of these remorins were analyzed and a remorin gene, CaREM1.4, was cloned for further study. The transcription of CaREM1.4 in pepper was induced by infection with Ralstonia solanacearum. Knocking down CaREM1.4 in pepper using virus-induced gene silencing (VIGS) technologies reduced the resistance of pepper plants to R. solanacearum and downregulated the expression of immunity-associated genes. Conversely, transient overexpression of CaREM1.4 in pepper and Nicotiana benthamiana plants triggered hypersensitive response-mediated cell death and upregulated expression of defense-related genes. In addition, CaRIN4-12, which interacted with CaREM1.4 at the plasma membrane and cell nucleus, was knocked down with VIGS, decreasing the susceptibility of Capsicum annuum to R. solanacearum. Furthermore, CaREM1.4 reduced ROS production by interacting with CaRIN4-12 upon co-injection in pepper. Taken together, our findings suggest that CaREM1.4 may function as a positive regulator of the hypersensitive response, and it interacts with CaRIN4-12, which negatively regulates plant immune responses of pepper to R. solanacearum. Our study provides new evidence for comprehending the molecular regulatory network of plant cell death.

TaBln1, a member of the Blufensin family, negatively regulates wheat resistance to stripe rust by reducing Ca2+ influx.

Blufensin1 (Bln1) has been identified as a susceptibility factor of basal defense mechanisms which is unique to the cereal grain crops barley (Hordeum vulgare), wheat (Triticum aestivum), rice (Oryza sativa), and rye (Secale cereale). However, the molecular mechanisms through which Bln1 regulates the wheat immune response are poorly understood. In this study, we found that TaBln1 was significantly induced by Puccinia striiformis f. sp. tritici (Pst) virulent race CYR31 infection. Knockdown of TaBln1 expression by virus-induced gene silencing reduced Pst growth and development, and enhanced the host defense response. In addition, TaBln1 was found to physically interact with a calmodulin, TaCaM3, on the plasma membrane. Silencing TaCaM3 with virus-induced gene silencing increased fungal infection areas and sporulation and reduced wheat resistance to the Pst avirulent race CYR23 (incompatible interaction) and virulent race CYR31 (compatible interaction). Moreover, we found that the accumulation of TaCaM3 transcripts could be induced by treatment with chitin but not flg22. Silencing TaCaM3 decreased the calcium (Ca2+) influx induced by chitin, but silencing TaBln1 increased the Ca2+ influx in vivo using a noninvasive micro-test technique. Taken together, we identified the wheat susceptibility factor TaBln1, which interacts with TaCaM3 to impair Ca2+ influx and inhibit plant defenses.