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Matsumura, E. E.

Publications and source records attributed to Matsumura, E. E..

2 recordsLinked to original sources

Stationary phloem proteins and their effects on viruses, aphids, and cyst nematodes in Arabidopsis

The phloem is a specialized tissue that facilitates systemic transport of carbohydrates and signal molecules, making it a common target for viruses, phloem-feeding insects, and cyst nematodes. In Arabidopsis, the stationary phloem-associated SIEVE ELEMENT-LINING CHAPERONE1 (SLI1) and RESTRICTED TEV MOVEMENT (RTM) proteins restrict insect phloem-feeding and potyviruses systemic transport, respectively. However, their broader roles in plant-attacker interactions remain largely unexplored. We investigated the roles of SLI1, RTM1, RTM2, and RTM3 in tobacco etch virus (TEV) infection, as well as in Myzus persicae and Heterodera schachtii infestations using Arabidopsis mutants. Systemic TEV movement was quantified, aphid behaviour and reproduction were assessed, and cyst nematode infection was monitored. SLI1 did not restrict TEV systemic movement, RTM3 reduced M. persicae reproduction without altering feeding behaviour, SLI1, RTM2, and RTM3 supported H. schachtii infection and feeding site expansion, and confocal images indicated a possible role of the proteins in de novo synthesis of sieve tubes around syncytia. These findings reveal that stationary phloem proteins exert dual and target-specific effects, limiting some attackers while inadvertently facilitating others. This highlights the complexity of phloem-based immunity and underscores the need to unravel its underlying mechanisms to develop strategies to reduce multiple pest and pathogen burdens simultaneously. HighlightStationary phloem proteins SLI1, RTM1, RTM2, and RTM3 exert dual and target-specific effects against tobacco etch virus, Myzus persicae, and Heterodera schachtii.

plant biology↗

Development of a cricket paralysis virus-based system for inducing RNA interference-mediated gene silencing in Diaphorina citri

Diaphorina citri, the Asian citrus psyllid, is the insect vector of the phloem-limited bacterium Candidatus Liberibacter asiaticus, which causes the most devastating citrus disease worldwide: Huanglongbing (HLB). An efficient cure for HLB is still not available and the management of the disease is restricted to the use of pesticides, antibiotics and eradication of infected plants. Plant- and insect-infecting viruses have attracted increasing attention for their potential to manipulate traits in insects, especially insect vectors of plant pathogens. However, so far there are no insect virus-based vectors available for use in D. citri. Cricket paralysis virus (CrPV) is a well-studied insect-infecting dicistrovirus with a wide host range and has been used as a model in previous translational studies. In this work, we demonstrate for the first time that CrPV is infectious and pathogenic to D. citri. We show that specific amino acid mutations in the CrPV primary cleavage DvExNPGP motif resulted in a viral mutant that was attenuated compared to wild-type CrPV during infection of either Drosophila cells line or adult D. citri insects. This attenuated CrPV mutant was then used as the backbone for engineering a recombinant CrPV-based vector to specifically alter D. citri gene expression via the RNA interference (RNAi) pathway, a technology called Virus Induced Gene Silencing (VIGS). As proof-of-concept, we engineered recombinant CrPV-based vectors carrying nucleotide sequences derived from a previously reported D. citri target gene: the inhibitor of apoptosis gene (IA). RT-qPCR analysis of insects either microinjected or fed with the recombinant CrPV mutants showed decreased IA gene expression as soon as viral replication was detected, indicating that the engineered CrPV-based VIGS system enables functional gene silencing in D. citri. This novel insect virus-based tool is easily amenable to genomic modification and represents a technical advance for understanding interactions between insect virus-based VIGS systems and D. citri.

molecular biology↗