RESUMEN
The nucleolus is conventionally acknowledged for its role in ribosomal RNA (rRNA) synthesis and ribosome biogenesis. Recent research has revealed its multifaceted involvement in plant biology, encompassing regulation of the cell cycle, development, and responses to environmental stresses. This comprehensive review explores the diverse roles of the nucleolus in plant growth and responses to environmental stresses. The introduction delves into its traditional functions in rRNA synthesis and potential participation in nuclear liquid-liquid phase separation. By examining the multifaceted roles of nucleolar proteins in plant development, we highlight the impacts of various nucleolar mutants on growth, development, and embryogenesis. Additionally, we reviewed the involvement of nucleoli in responses to abiotic and biotic stresses. Under abiotic stress conditions, the nucleolar structure undergoes morphological changes. In the context of biotic stress, the nucleolus emerges as a common target for effectors of pathogens for manipulation of host immunity to enhance pathogenicity. The detailed exploration of how pathogens interact with nucleoli and manipulate host responses provides valuable insights into plant stress responses as well as plant growth and development. Understanding these processes may pave the way for promising strategies to enhance crop resilience and mitigate the impact of biotic and abiotic stresses in agricultural systems.
RESUMEN
Transient and rapid increase in cytosolic Ca2+ plays a crucial role in plant-pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI). Cyclic nucleotide-gated channels (CNGCs) have been implicated in mediating this Ca2+ influx; however, their regulatory mechanisms remain poorly understood. Here, we have found that AVRblb2 requires the calmodulin (CaM) and calmodulin-like (CML) proteins as co-factors to interact with the NbCNGCs, resulting in the formation of AVRblb2-CaM/CML-NbCNGCs complex. Furthermore, CaM and CML are dissociated from NbCNGC18 during PTI response to increase Ca2+ influx; however, Avrblb2 inhibits calcium channel activation by disrupting the release of CaM and CML from NbCNGC18. Following recognition of PAMP, NbCNGC18 forms active heteromeric channels with other NbCNGCs, which may give selectivity of CNGC complex against diverse signals for fine-tuning of cytosolic Ca2+ level to mediate appropriate responses. Silencing of multiple NbCNGCs compromised the function of AVRblb2 on the pathogenicity of Phytophthora infestans, confirming that AVRblb2 contributes to pathogen virulence by targeting CNGCs. Our findings provide new insights into the regulation of CNGCs in PTI and the role of pathogen effectors in manipulating host cell physiology to promote infection.
Asunto(s)
Calmodulina , Phytophthora infestans , Calmodulina/metabolismo , Canales Catiónicos Regulados por Nucleótidos Cíclicos/metabolismo , Calcio/metabolismo , Reconocimiento de Inmunidad Innata , Phytophthora infestans/metabolismo , Nucleótidos Cíclicos/metabolismo , Inmunidad de la PlantaRESUMEN
Some nucleotide-binding and leucine-rich repeat receptors (NLRs) indirectly detect pathogen effectors by monitoring their host targets. In Arabidopsis thaliana, RIN4 is targeted by multiple sequence-unrelated effectors and activates immune responses mediated by RPM1 and RPS2. These effectors trigger cell death in Nicotiana benthamiana, but the corresponding NLRs have yet not been identified. To identify N. benthamiana NLRs (NbNLRs) that recognize Arabidopsis RIN4-targeting effectors, we conducted a rapid reverse genetic screen using an NbNLR VIGS library. We identified that the N. benthamiana homolog of Ptr1 (Pseudomonas tomato race 1) recognizes the Pseudomonas effectors AvrRpt2, AvrRpm1, and AvrB. We demonstrated that recognition of the Xanthomonas effector AvrBsT and the Pseudomonas effector HopZ5 is conferred independently by the N. benthamiana homolog of Ptr1 and ZAR1. Interestingly, the recognition of HopZ5 and AvrBsT is contributed unequally by Ptr1 and ZAR1 in N. benthamiana and Capsicum annuum. In addition, we showed that the RLCK XII family protein JIM2 is required for the NbZAR1-dependent recognition of AvrBsT and HopZ5. The recognition of sequence-unrelated effectors by NbPtr1 and NbZAR1 provides an additional example of convergently evolved effector recognition. Identification of key components involved in Ptr1 and ZAR1-mediated immunity could reveal unique mechanisms of expanded effector recognition.
Asunto(s)
Proteínas de Arabidopsis , Arabidopsis , Arabidopsis/metabolismo , Proteínas/metabolismo , Bacterias/metabolismo , Proteínas Portadoras/metabolismo , Pseudomonas , Receptores Inmunológicos/metabolismo , Proteínas Bacterianas/metabolismo , Pseudomonas syringae/metabolismo , Enfermedades de las Plantas/microbiología , Proteínas de Arabidopsis/metabolismo , Péptidos y Proteínas de Señalización Intracelular/metabolismoRESUMEN
Pathogen effectors target diverse subcellular organelles to manipulate the plant immune system. Although the nucleolus has emerged as a stress marker and several effectors are localized in the nucleolus, the roles of nucleolar-targeted effectors remain elusive. In this study, we showed that Phytophthora infestans infection of Nicotiana benthamiana results in nucleolar inflation during the transition from the biotrophic to the necrotrophic phase. Multiple P. infestans effectors were localized in the nucleolus: Pi23226 induced cell death in N. benthamiana and nucleolar inflation similar to that observed in the necrotrophic stage of infection, whereas its homolog Pi23015 and a deletion mutant (Pi23226ΔC) did not induce cell death or affect nucleolar size. RNA immunoprecipitation and individual-nucleotide-resolution UV crosslinking and immunoprecipitation sequencing analysis indicated that Pi23226 bound to the 3' end of 25S rRNA precursors, resulting in accumulation of unprocessed 27S pre-rRNAs. The nucleolar stress marker NAC082 was strongly upregulated under Pi23226-expressing conditions. Pi23226 subsequently inhibited global protein translation in host cells by interacting with ribosomes. Pi23226 enhanced P. infestans pathogenicity, indicating that Pi23226-induced ribosome malfunction and cell death were beneficial for pathogenesis in the host. Our results provide evidence for the molecular mechanism underlying RNA-binding effector activity in host ribosome biogenesis and lead to new insights into the nucleolar action of effectors in pathogenesis.