BSPP News Spring 2002 - Online Edition

The Newsletter of the British Society for Plant Pathology
Number 41, Spring 2002

Rhizomania in the news

Rhizomania of sugar beet has been in the news recently due to a sudden upsurge in the number of new outbreaks recorded last year and the consequences of this for the UK's long standing control policy for this disease.  Since the first outbreak in 1987, MAFF/DEFRA have successfully negotiated with our EU partners for Protected Zone status for rhizomania in this country.  As part of this, import controls require, among other things, that plant material for transplanting that might carry soil (e.g. seed potatoes) must be from certified rhizomania-free areas, and soil limits are imposed on some vegetables imported for consumption.  As a consequence, in this country rhizomania is a notifiable disease under statutory control.  Extensive surveys are carried out each year to detect the disease, infected crops or parts of crops are destroyed in situ and sugar beet cropping on infested fields is prohibited.

So why the concern with this disease?  Rhizomania, caused by Beet necrotic yellow vein virus and transmitted by the plasmodiophorid root parasite, Polymyxa betae, exhibits several unusual features.  Firstly, the resting spores of the fungus (or protist? - this is currently under debate) which harbour the virus persist almost indefinitely in soil.  Essentially, unlike most soil-borne pests and pathogens, inoculum does not decline in the absence of host crops and cannot be eliminated artificially (e.g. by fumigation).  Secondly, inoculum multiplication in susceptible host crops (primarily Beta species) can be extremely rapid.  A ten thousand fold increase in soil inoculum potential during one cropping season, and over a million fold following two successive crops, has been demonstrated experimentally.

Because of this the disease is very easily spread; only small amounts of soil on farm machinery, planting material, or spread by wind, are required to contaminate other fields or farms.  Up until recently, prior to the introduction of the first partially resistant cultivars, there has been no means of controlling rhizomania once a field was contaminated.  Finally, of course, once established the disease has the potential to severely damage root growth, causing the proliferation of fibrous lateral roots (see photo) (the root madness symptom after which the disease is named) at the expense of the tap root; yield losses of 60-70% are the norm.

Bearding induced by Rhizomania

In this country the disease has developed relatively slowly compared with most countries in continental Europe, due largely to our less favourable climate and the policy of containment adopted to slow its spread.  Up to now it has been recorded on 7300 ha on just over 200 farms, mainly confined to the light sandy soils on which sugar beet is grown in East Anglia.  This constitutes about 1 per cent of the total sugar-beet growing land in the UK.  In contrast, in the countries of continental Western Europe over 700 k ha of sugar-beet crops were infected with rhizomania in the year 2000 alone, and the disease is also widespread in Japan, China and the USA.

Clearly, given that it is impossible to prevent its continued spread, the use of resistant cultivars offers the best long-term solution to the problem.  Breeders have made great progress over the past 10-15 years and cultivars derived from a single monogenic source of partial resistance to the virus are now widely grown in continental Europe and the USA.  Currently, however, only one of these cultivars is agronomically suited to UK conditions.  Other potential sources of resistance have been identified in wild Beta species, even among the wild sea beet (B. maritima) populations from our own coastline.  However, none as yet has been found to confer a level of resistance equivalent to that achieved against the cereal soil-borne viruses.  Transgenic approaches, exploiting the coat-protein and movement genes of the virus, have also shown promise, but await public acceptance!  Resistance to the fungal vector is a particular interest of our group.

So what of the future?  With the number of farms now affected in East Anglia it seems unlikely that this region can any longer be included as part of the Protected Zone.  At the time of writing, whether the remainder of the country persists with this policy remains to be decided.  Meanwhile, there is a continuing flow of resistant cultivars going through trials.  Several of these are likely to offer an economically viable option on affected farms over the next few years but, in the longer term, improved and potentially more durable resistance is needed.

Mike Asher
IACR-Broom's Barn

David Baulcombe FRS 

David Baulcombe, a Senior Scientist at the Sainsbury Laboratory, Norwich and currently Head of the Laboratory, was elected a Fellow of the Royal Society on 14th May 2001. He is the first scientist working in plant pathology to be elected an FRS for over ten years. David began his scientific career at the Plant Breeding Institute, Cambridge, as part of the team working on molecular genetics of wheat. At that time, he pursued a side interest in virology, one attraction being that these experiments took weeks rather than the years needed for research on wheat genetics. In 1989, he had the opportunity to make research on viral diseases his full-time occupation by moving to the Sainsbury Laboratory, where he became one of its first three Senior Scientists.

In the citation which marked his election as a Fellow, the Royal Society said, "David Baulcombe has made an outstanding contribution to the inter-related areas of plant virology, gene silencing and disease resistance. He discovered a specific signalling system and an antiviral defence system in plants. This led to the development of new technologies that promise to revolutionise gene discovery in plant biology."

Virus-induced gene silencing

Although he describes himself as "a humble seeker of the truth", David has contributed enormously to our understanding of plant science His work on virus-induced gene silencing has brought together two areas of research which were not previously thought to be connected, induced resistance to disease and gene silencing. Induced resistance is, of course, familiar to pathologists from the early work by Joseph Kuc onwards. Post-transcriptional gene silencing, also known as RNA silencing, is a more recent discovery, made in the last decade or so. The original observation was that a transgene could suppress the expression of a second, similar gene in the same genome.

The starting point of David's ground-breaking research was two papers in which his group showed that viruses could be a target of RNA silencing (Plant J. 1995, 7:1001-13; Plant Cell 1996, 8:179-88). In subsequent experiments, they have made significant progress towards unravelling the mechanism of RNA silencing and have showen that it is a general phenomenon, giving resistance to many viruses, retrotransposons and other alien nucleic acid species.

Following the observation that viruses may both initiate and be targets of RNA silencing, David's group showed that virus infection of non-transgenic plants induces a resistance mechanism similar to that of transgene-induced gene silencing (Science 1997, 276: 1558-60; Plant Cell 1999, 11:1207-15). The first paper is particularly significant in showing that leaves which develop after systemic infection of a plant by a virus contain lower concentrations of virus, are symptom-free and have essentially recovered. These leaves are then protected against subsequent infection by viruses with similar RNA sequences but not against unrelated viruses. The second of these papers showed that RNA-mediated defence is a general response to virus infection.

A fascinating aspect of systemic defence is the existence of a signal that moves ahead of the virus through the phloem. This was discovered by David's group in elegant grafting experiments, in which the signal moved from a silenced root-stock into a non-silenced scion (Cell 1998, 95:177-87).

Given that plants have this general system of protection against viruses, one might imagine that viruses would have evolved strategies to avoid or suppress the silencing mechanism. That this is indeed the case was confirmed when suppressors of RNA silencing were discovered in two viruses, which prevent either the initiation or the maintenance of silencing (EMBOJ. 1998: 17:6739-36).

A mechanism of silencing

These discoveries clearly implied that RNA silencing is sequence-specific. The next milestone was the discovery of small RNA species, approximately 25 bases in length and similar in sequence to the RNA which is targetted for silencing (Science 1999:286:950-2). These small interfering RNA species (SiRNA) have since been shown to be markers of RNA silencing throughout eukaryotes, with examples from fungi, insects and the nematode C. elegans, as well as several plants.

The power of Arabidopsis genomics then came to the fore as an RNA-dependent RNA polymerase gene, SDE1, was discovered (Cell 2000, 101:543-53). Here, an important difference between silencing induced by transgenes and by viruses was found as a functional SDE1 protein is only needed for the former process. SDE1 is thought to synthesise a double-stranded RNA which initiates silencing but the virus' own RNA polymerase produces a dsRNA, so that SDE1 may be redundant in this situation.

Resistance to viruses

David has other interests in virus resistance besides silencing, stemming from his long-term model system, potato virus X. The Rx gene of potato confers 'extreme resistance' to PVX, which does not involve cell death at the infection site. It was expected that Rx might represent a novel class of resistance genes but, when isolated, it turned out to be a member (yet another!) of the well-known group of NBS-LRR genes (Plant Cell 1999, 11:781-91). The lab is now focussing on genes required for the function of Rx resistance and on the function of the Rx protein.

A technology for gene discovery

David's interests in silencing and disease resistance are now being brought together in the development of virus-induced gene silencing (VIGS) as a powerful tool for identifying genes in plants. The basis of VIGS is that a plant is infected with a virus carrying a fragment of host sequence and the virus then spreads systemically. As the virus replicates in host cells, it causes silencing to be directed against host gene transcripts which have similar sequences to that of the virus (Curr Opinion in Plant Biol 1999, 2:109-13). Sequence-specificity means that VIGS is especially powerful because it allows the expression of whole gene families to be disrupted. 

VIGS is being used to isolate genes required for disease resistance but the system has a much broader range of applications. For example, the leafy gene, which is involved in determining meristem identity, has been disrupted (Plant J. 2001, 25:237-45), demonstrating the power of the VIGS technology in investigating problems far outside its origin in research on disease resistance. VIGS is potentially a powerful tool in biotechnology and David is taking an active role in the current debate on GM.

Keeping up with the postdocs

Considering that when David is not travelling, he spends much of his time cooped up in his office, he has an uncanny ability to keep up with exactly what is happening in his lab. His group is currently 20 strong so it is quite a talent. In part, he manages to do this by being so receptive to discussion - his office door is always open.

But he isn't stuck in the office the whole time and has many other interests. He sails, plays squash and jogs to keep in shape. At a Christmas party, the members of his lab were enjoying dinner at his house when one of them challenged him to a running race around a local lake. By the end of the evening, David bet that he could beat them all, offering stakes of pizza and a round of drinks for the whole lab. Although he came only third out of six, he then showed his competitive streak by challenging the younger members of his lab to another race before they could finish their first slice of pizza!

By several Baulcombe Lab members, with James Brown