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Janakowski, S.

Publications and source records attributed to Janakowski, S..

2 recordsLinked to original sources

Resistance Breaking in Root-knot Nematodes Carries a Fitness Cost Associated with Defective Feeding Site Development

Root-knot nematodes (RKNs) cause an estimated 157 billion dollars in annual yield losses worldwide. In tomato, resistance to RKNs is conferred by the single dominant resistance gene Mi-1, which has been widely integrated into commercial cultivars. Prolonged and widespread use of Mi-1 has led to the emergence of resistance-breaking populations in tomato fields worldwide; however, the consequences of resistance breaking for nematode performance on susceptible hosts remain poorly understood. Here, we compared infection outcomes of two closely related strains of Meloidogyne javanica, VW4 (Mi-1-avirulent; wild-type) and VW5 (Mi-1-virulent; resistance-breaking), on three susceptible hosts: tomato, cucumber, and rice. Across all hosts, VW5 produced significantly fewer eggs than VW4, revealing a fitness cost associated with Mi-1 virulence. Light and transmission electron microscopy of tomato and cucumber galls revealed impaired feeding site establishment by VW5. Consistent with these observations, transcriptomic profiling showed that VW5 infection induced weaker host transcriptional reprogramming and lacked gene expression signatures associated with effective suppression of plant defense responses. Together, these findings demonstrate that adaptation to Mi-1-mediated resistance incurs a fitness cost on susceptible plants and is accompanied by impaired feeding site formation and altered host reprogramming. Furthermore, these results establish VW4 and VW5 as a powerful resource for understanding nematode genes and pathways required for successful parasitism and feeding site development.

plant biology↗

The genome and lifestage-specific transcriptomes of a plant-parasitic nematode and its host reveal susceptibility genes involved in trans-kingdom synthesis of vitamin B.

Plant-parasitic nematodes are a major, and in some cases a dominant, threat to crop production in all agricultural systems. The relative scarcity of classical resistance genes highlights a pressing need to identify new ways to develop nematode-resistant germplasm. Here, we sequence and assemble a high-quality genome of the model cyst nematode Heterodera schachtii to provide a platform for the first system-wide dual analysis of host and parasite gene expression over time, covering all major stages of the interaction. This novel approach enabled the analysis of the hologenome of the infection site, to identify metabolic pathways that were incomplete in the parasite but complemented by the host. Using a combination of bioinformatic, genetic, and biochemical approaches, we show that the highly atypical completion of vitamin B5 biosynthesis by the parasitic animal, putatively enabled by a horizontal gene transfer from a bacterium, is critically important for parasitism. Knockout of either the plant-encoded or the now nematode-encoded steps in the pathway blocks parasitism. Our experiments establish a reference for cyst nematodes, use this platform to further our fundamental understanding of the evolution of plant-parasitism by nematodes, and show that understanding congruent differential expression of metabolic pathways represents a new way to find nematode susceptibility genes, and thereby, targets for future genome editing-mediated generation of nematode-resistant crops.

genetics↗