If only there was a police force for sugar beet...? Probably not, but Mark McMullan and Michelle Grey are working out the science behind some of the deadly diseases of sugar beet, using its wild relative - sea beet - to explore how plant pathogens become so well adapted to their agricultural hosts.
There’s nothing quite like the smell that hits your nostrils quite abruptly as you approach Bury St. Edmunds (along the A134 road) from the direction of the A11 at Thetford: the pongy whiff of crushed beet combined with sickly sweet, possibly singed, syrupy sugar. Some find it delicious (me and my invisible friend), others in the office disagree with us entirely (they’re all wrong!)
Sugar beet is a very important crop for the East Anglia region and elsewhere in the UK, with huge sugar factories dotting the landscape, in addition to fields teeming with the plants themselves. However, we’re not going to talk about the effect of deadly diseases on the economic wellbeing of the sugar industry - as important as that is.
In fact, Dr Mark McMullan, of the Neil Hall Group at EI - while endeavouring to hunt for novel forms of resistance to help sugar beet survive new pathogen threats - is particularly interested in sugar beet from a more wide-reaching angle: one which could give us a far greater understanding of the threats to each and every one of our crops.
You see, for many years, we have been studying agricultural pathogens without really understanding their wild progenitors.
As one of our most recently domesticated crops, sugar beet is really interesting to study; compared to wheat it’s an agricultural baby. Wheat was domesticated around 13,000 years ago in the Fertile Crescent, while beet was only domesticated between 200-400 years ago in Poland.
Sea beet, the wild relative of sugar beet, as well as living in close proximity to its domesticated cousins, also shares many of its diseases. This is extremely interesting, as it provides a unique example to explore the evolution of plant pathogens before they really have the chance to diverge.
You see, for many years, we have been studying agricultural pathogens without really understanding their wild progenitors. Mark thinks that this means that we have been largely missing what makes an agricultural pathogen so effective.
In crop breeding and genomics, the oft-proposed perspective is that we need to introduce variation from the wild relatives of crops. Crop domestication through breeding has inadvertently removed a lot of genetic variation. Therefore, to help crops withstand the diseases rampant in agriculture, we breed in novel sources of resistance that are still evolving in the wild hosts.
This is fine, but probably only tells half of the story. What if there is variation that we’re missing?
There are plenty of diseases that don’t traverse the wild-agricultural boundary. What is the difference between those that don’t and those that do?
It’s only by looking at the pathogens of wild relatives of plants, such as sea beet, and comparing them to their agricultural counterparts such as sugar beet and beetroot, that we can properly identify what makes a successful agricultural disease.
Sea beet, the wild relative of sugar beet, as well as living in close proximity to its domesticated cousins, also shares many of its diseases. This is extremely interesting, as it provides a unique example to explore the evolution of plant pathogens before they really have the chance to diverge.
To fully understand what’s going on in our fields, we must look into the wild. We already know from looking at ash dieback disease that a pathogen, when invading a new range, starts with a low diversity - perhaps from just a single spore.
Successive waves, bolstered by new variation from further afield, can then really cement the problem. When looking at sea beet and sugar beet, this process is reciprocal, at least currently, as the domestication process was so recent.
That’s why sea beet is so interesting to study: we can go digging around on the Suffolk coast and find wild plants that are living mere miles from sugar beet fields, sharing the same sorts of diseases with their domesticated counterparts.
We get a snapshot in the evolution of agricultural pathogens. What if there’s information that we can glean from the strains of beet rust that affect domestic beet, but not wild beet? What if we can add this information to the mix when it comes to understanding how to breed resistance to crop diseases?
However, early data suggests that there are some parts of the genome that are not shared by the strains present on either lineage of crops.
So, the only thing to do is to go out and get some samples of diseased wild beet, bring them back to the lab, sequence them, genotype them, and compare them with the same diseases found on domesticated beet.
Currently, the diseases under the spotlight are beet rust and powdery mildew, the agricultural and wild forms of which do look very similar, genetically speaking, in domestic and wild beet. However, early data suggests that there are some parts of the genome that are not shared by the strains present on either lineage of crops.
It’s most likely those parts, that will tell us what makes a good agricultural pathogen.
The next step is to identify potential genes in these regions, or even spot the non-coding elements that can also affect the fitness of the disease, and likelihood to attack a domestic beet or a wild beet.
Then, the next stage would be to identify resistance in the host.
Already, the team has started the search for the presence of these processes in wheat root fungi.
So, the only thing to do is to go out and get some samples of diseased wild beet, bring them back to the lab, sequence them, genotype them, and compare them with the same diseases found on domesticated beet.
We don’t really know that much at all about the origins of agricultural pathogens and diseases, little about their wild relatives or progenitors, and we domesticated most of our crops so many thousands of years ago that it becomes difficult to understand precisely their evolutionary journey and divergence.
The implications are very interesting when it comes to protecting our crops. Perhaps, as important as it may be to breed resistance and variety into our crops, we would be just as well understanding the evolution of pathogens as a whole. Where does new diversity arise? How can we can precisely defend crops in specific areas or regions.
We might discover, for example, that breeding in resistance from wild relatives of crops is simply a short term fix. What if our agricultural diseases then breed with their own wild relatives in adjacent fields? It’s more than likely. Wheat yellow rust has its sexual phase on barbery, therefore it isn’t hard to suppose that many of the diseases of our crops have the chance to expand their genetic armoury far (or not so far) from our pesticide and fungicide-laden fields.
We’re talking beet here (it’s a lot easier to study beet in Norfolk) but what we can find out about beet from its wild ancestor sea beet could easily be applied to the study of wheat in the Fertile Crescent, where its own closely related wild ancestors are found.
It’s early days, and there are many years of research to be done to even begin to unravel the processes that shape the evolution of crop pathogens. However, with modern genomics, we’re getting closer to making a much fuller picture, that can only help to bolster efforts to understand how best we can protect our crops and our food.
We might discover, for example, that breeding in resistance from wild relatives of crops is simply a short term fix.
