Flexible growth and immune responses in rice: Plants that are fighting microbial pathogens often divert resources that could be used for growth into the immune response. For crops, this translates into lower yield when plant immunity is activated. Wang et al. show that, in rice, reversible phosphorylation of a key transcription factor allows the plant to defend against fungal attack when needed but then, within days, reallocate resources back to growth (see the Perspective by Greene and Dong). Thus, both pathogen defense and crop yield can be sustained. Science , this issue p. 1026 ; see also p. 976

The plant cell wall is the first physical and defensive barrier against pathogens. The plant cell wall usually undergoes dynamic remodeling as an immune response to prevent infection by pathogens. In this review, we summarize advances on relationship between cell wall and immunity in plants. In particular, we outline current progresses regarding the regulation of the cell wall components, including cellulose, hemicellulose, pectin and lignin, on plant disease resistance. We also discuss the impacts of cell wall-derived cellodextrin, oligogalacturonic acid and xyloglucan/xylan oligosaccharides as potent elicitors or signal molecules to trigger plant immune response. We further propose future studies on dissecting the molecular regulation of cell wall on plant immunity, which have potentials in practical application of crop breeding aiming at improvement of plant disease resistance.

Significance: Crops carrying broad-spectrum resistance loci provide an effective strategy for controlling infectious disease. Despite their importance, few broad-spectrum resistance loci have been reported, and the underlying mechanisms controlling the trait remain largely unknown. This report describes the identification of a gene, called “ bsr-k1 ,” conferring broad-spectrum resistance and demonstrates that the encoded protein regulates immunity-related genes. Loss of function of BSR-K1 in rice leads to enhanced broad-spectrum resistance to two serious rice diseases with no major penalty on yield. This report provides insights into broad-spectrum resistance and offers an efficient strategy to breeding durably resistant rice.

Blast is arguably the most devastating fungal disease of rice. Systematic studies of this disease have made significant progress and identified many genes. Broad-spectrum resistance is highly preferred in agricultural practice. Here, we focus our discussion on resistance (R) and defense-regulator (DR) genes that confer broad-spectrum resistance to Magnaporthe oryzae, in particular those potentially causing no significant yield penalties. Recent advances show that broad-spectrum resistance can be achieved without significant yield penalties, or even with yield benefits. Cross talks of defense signaling mediated by these genes are present that may allow the host to integrate different anti-fungal factors against M. oryzae infection. We also summarize possible mechanisms underlying broad-spectrum resistance to rice blast.

The rice XA21 immune receptor kinase and the structurally related XA3 receptor confer immunity to Xanthomonas oryzae pv. oryzae (Xoo), the causal agent of bacterial leaf blight. Here we report the isolation of OsSERK2 (rice somatic embryogenesis receptor kinase 2) and demonstrate that OsSERK2 positively regulates immunity mediated by XA21 and XA3 as well as the rice immune receptor FLS2 (OsFLS2). Rice plants silenced for OsSerk2 display altered morphology and reduced sensitivity to the hormone brassinolide. OsSERK2 interacts with the intracellular domains of each immune receptor in the yeast two-hybrid system in a kinase activity-dependent manner. OsSERK2 undergoes bidirectional transphosphorylation with XA21 in vitro and forms a constitutive complex with XA21 in vivo. These results demonstrate an essential role for OsSERK2 in the function of three rice immune receptors and suggest that direct interaction with the rice immune receptors is critical for their function. Taken together, our findings suggest that the mechanism of OsSERK2-meditated regulation of rice XA21, XA3, and FLS2 differs from that of AtSERK3/BAK1-mediated regulation of Arabidopsis FLS2 and EFR.