Molecular plant pathology最新文献

Phytoplasmas are phloem-restricted plant-pathogenic bacteria transmitted by insects. They cause diseases in a wide range of host plants, resulting in significant economic and ecological losses worldwide. Research on phytoplasmas has a long history, with significant progress being made in the past 30 years. Notably, with the rapid development of phytoplasma research, scientists have identified the primary agents involved in phytoplasma transmission, established classification and detection systems for phytoplasmas, and 243 genomes have been sequenced and assembled completely or to draft quality. Multiple possible phytoplasma effectors have been investigated, elucidating the molecular mechanisms by which phytoplasmas manipulate their hosts. This review summarizes recent advances in phytoplasma research, including identification techniques, host range studies, whole- or draft-genome sequencing, effector pathogenesis and disease control methods. Additionally, future research directions in the field of phytoplasma research are discussed.

Viruses rely completely on host translational machinery to produce the proteins encoded by their genes. Controlling translation initiation is important for gaining translational advantage in conflicts between the host and virus. The eukaryotic translation initiation factor 4E (eIF4E) has been reported to be hijacked by potyviruses for virus multiplication. The role of translation regulation in defence and anti-defence between plants and viruses is not well understood. We report that the transcript level of eIF6 was markedly increased in turnip mosaic virus (TuMV)-infected Nicotiana benthamiana. TuMV infection was impaired by overexpression of N. benthamiana eIF6 (NbeIF6) either transiently expressed in leaves or stably expressed in transgenic plants. Polysome profile assays showed that overexpression of NbeIF6 caused the accumulation of 40S and 60S ribosomal subunits, the reduction of polysomes, and also compromised TuMV UTR-mediated translation, indicating a defence role for upregulated NbeIF6 during TuMV infection. However, the polysome profile in TuMV-infected leaves was not identical to that in leaves overexpressing NbeIF6. Further analysis showed that TuMV NIb protein, the RNA-dependent RNA polymerase, interacted with NbeIF6 and interfered with its effect on the ribosomal subunits, suggesting that NIb might have a counterdefence role. The results propose a possible regulatory mechanism at the translation level during plant-virus interaction.

Niu Y, Fu S, Chen G, Wang H, Wang Y, Hu J, Jin X, Zhang M, Lu M, He Y, Wang D, Chen Y, Zhang Y, Coll N, Valls M, Zhao C, Chen Q and Lu H. Different epitopes of Ralstonia solanacearum effector RipAW are recognized by two Nicotiana species and trigger immune responses. Molecular Plant Pathology 2022;23:188–203

In the authorship section, the affiliations ‘Dongdong Wang², Yong Zhang^3,4, Núria S. Coll⁵, Marc Valls^5,6, Qin Chen² and Haibin Lu^1,7’ (Author's affiliations) were incorrect. They should have read ‘Dongdong Wang³, Yong Zhang^4,5, Núria S. Coll⁶, Marc Valls^6,7, Qin Chen³ and Haibin Lu^1,2’

We apologize for these errors.

Mansi, Kushwaha, N.K., Singh, A.K., Karim, M.J. and Chakraborty, S. (2019) Nicotiana benthamiana phosphatidylinositol 4-kinase type II regulates chilli leaf curl virus pathogenesis. Molecular Plant Pathology, 20(10), 1408–1424. https://doi.org/10.1111/mpp.12846.

In the published version of this article in Figure 6, panels (d) and (e) were mistakenly used for both the NbPI4KII-mGFP + Rep1-180-DsRed and NbPI4KII-mGFP + Rep181-361-DsRed images. The two panels showing individual microscopy images with the NbPI4KII-mGFP + Rep1-180-DsRed and NbPI4KII-mGFP + Rep181-361-DsRed are highly identical; hence this mistake happened during figure assembly. This inadvertent figure error does not in any way alter the interpretations or the conclusions drawn in the manuscript. The corrected Figure 6 is shown below.

We apologize for this error.

Root-knot nematodes (RKNs) inflict extensive damage to global agricultural production. Intercropping has been identified as a viable agricultural tool for combating RKNs, but the mechanisms by which intercropped plants modulate RKN parasitism are still not well understood. Here, we focus on the cucumber-amaranth intercropping system. We used a range of approaches, including the attraction assay, in vitro RNA interference (RNAi), untargeted metabolomics, and hairy root transformation, to unveil the mechanisms by which weak host plants regulate Meloidogyne incognita chemotaxis towards host plants and control infection. Amaranth roots showed a direct repellence to M. incognita through disrupting its chemotaxis. The in vitro RNAi assay demonstrated that the Mi-flp-1 and Mi-flp-18 genes (encoding FMRFamide-like peptides) regulated M. incognita chemotaxis towards cucumber and controlled infection. Moreover, M. incognita infection stimulated cucumber and amaranth to accumulate distinct metabolites in both root tissues and rhizosphere soils. In particular, naringenin and salicin, enriched specifically in amaranth rhizosphere soils, inhibited the expression of Mi-flp-1 and Mi-flp-18. In addition, overexpression of genes involved in the biosynthesis of pantothenic acid and phloretin, both of which were enriched specifically in amaranth root tissues, delayed M. incognita development in cucumber hairy roots. Together, our results reveal that both the distinct host status and disruption of chemotaxis contribute to M. incognita inhibition in intercropping.