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Open Access Research

Phytophthora capsici-tomato interaction features dramatic shifts in gene expression associated with a hemi-biotrophic lifestyle

Julietta Jupe12, Remco Stam123, Andrew JM Howden12, Jenny A Morris23, Runxuan Zhang4, Pete E Hedley23* and Edgar Huitema12*

Author affiliations

1 Division of Plant Sciences, University of Dundee, Dundee DD2 5DA, UK

2 Dundee Effector Consortium, James Hutton Institute, Invergowrie, Dundee DD2 5DA, UK

3 Cell and Molecular Sciences, James Hutton Institute, Invergowrie, Dundee DD2 5DA, UK

4 Information and Computational Sciences, James Hutton Institute, Invergowrie, Dundee DD2 5DA, UK

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Citation and License

Genome Biology 2013, 14:R63  doi:10.1186/gb-2013-14-6-r63

Published: 25 June 2013

Abstract

Background

Plant-microbe interactions feature complex signal interplay between pathogens and their hosts. Phytophthora species comprise a destructive group of fungus-like plant pathogens, collectively affecting a wide range of plants important to agriculture and natural ecosystems. Despite the availability of genome sequences of both hosts and microbes, little is known about the signal interplay between them during infection. In particular, accurate descriptions of coordinate relationships between host and microbe transcriptional programs are lacking.

Results

Here, we explore the molecular interaction between the hemi-biotrophic broad host range pathogen Phytophthora capsici and tomato. Infection assays and use of a composite microarray allowed us to unveil distinct changes in both P. capsici and tomato transcriptomes, associated with biotrophy and the subsequent switch to necrotrophy. These included two distinct transcriptional changes associated with early infection and the biotrophy to necrotrophy transition that may contribute to infection and completion of the P. capsici lifecycle

Conclusions

Our results suggest dynamic but highly regulated transcriptional programming in both host and pathogen that underpin P. capsici disease and hemi-biotrophy. Dynamic expression changes of both effector-coding genes and host factors involved in immunity, suggests modulation of host immune signaling by both host and pathogen. With new unprecedented detail on transcriptional reprogramming, we can now explore the coordinate relationships that drive host-microbe interactions and the basic processes that underpin pathogen lifestyles. Deliberate alteration of lifestyle-associated transcriptional changes may allow prevention or perhaps disruption of hemi-biotrophic disease cycles and limit damage caused by epidemics.