Abstract

The root parasitic plant species Phelipanche ramosa, branched broomrape, causes severe damage to economically important crops such as tomato. Its seed germination is triggered by host-derived signals upon which it invades the host root. In tomato, strigolactones (SLs) are the main germination stimulants for P. ramosa. Therefore, the development of low SL-producing lines may be an approach to combat the parasitic weed problem. However, since SLs are also a plant hormone controlling many aspects of plant development, SL deficiency may also have an effect on post-germination stages of the infection process, during the parasite-host interaction. In this study, we show that SL-deficient tomato plants (Solanum lycopersicum; SlCCD8 RNAi lines), infected with pre-germinated P. ramosa seeds, display an increased infection level and faster development of the parasite, which suggests a positive role for SLs in the host defense against parasitic plant invasion. Furthermore, we show that SL-deficient tomato plants lose their characteristic SL-deficient phenotype during an infection with P. ramosa through a reduction in the number of internodes and the number and length of secondary branches. Infection with P. ramosa resulted in increased levels of abscisic acid (ABA) in the leaves and roots of both wild type and SL-deficient lines. Upon parasite infection, the level of the conjugate ABA-glucose ester (ABA-GE) also increased in leaves of both wild type and SL-deficient lines and in roots of one SL-deficient line. The uninfected SL-deficient lines had a higher leaf ABA-GE level than the wild type. Despite the high levels of ABA, stomatal aperture and water loss rate were not affected by parasite infection in the SL-deficient line, while in wild type tomato stomatal aperture and water loss increased upon infection. Future studies are needed to further underpin the role that SLs play in the interaction of hosts with parasitic plants and which other plant hormones interact with the SLs during this process.

Highlights

  • During evolution, parasitic plants have evolved a mechanism to infect and rely on other plant species’ water and nutrients for their growth and survival

  • We demonstrate a protective role for endogenous SLs after attachment of P. ramosa to tomato by comparing two independent SL-deficient SlCCD8 RNAi lines with the corresponding wild type

  • Because we were interested in differences in parasite attachment levels that were not the result of differences in P. ramosa seed germination, the parasitic plant seeds were pre-germinated, using the synthetic strigolactone analog GR24, before they were applied to the tomato roots

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Summary

Introduction

Parasitic plants have evolved a mechanism to infect and rely on other plant species’ water and nutrients for their growth and survival. The life cycle of P. ramosa consists of several different stages. These parasites have evolved a mechanism ensuring that they only germinate within the hosts’ rhizosphere. This feature is very important since they cannot survive long after germination unless they reach their hosts’ root. As the development of the vascular connection proceeds, a swollen organ, called a tubercle, is formed on the surface of the host root, enabling the accumulation of nutrients supporting further development of the parasite seedling. The shoots of mature parasitic plants emerge above the soil (Xie et al, 2010; Cardoso et al, 2011)

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