Wheat disease genes

Fusarium graminearum is the fungus that causes Fusarium head blight, a serious disease of wheat and barley. FHB infects the flowers and makes itself at home in the seed, which ends up shrunken and white and loaded with toxins that can have a harmful effect on people and animals that eat the grain. A study just published in Science decoded the DNA sequence of the fungus and sheds some light on its virulence and variability ((The Fusarium graminearum Genome Reveals a Link Between Localized Polymorphism and Pathogen Specialization. Science: 317:1400 – 1402 DOI: 10.1126/science.1143708)).

The sequence of one strain is interesting enough, but the surprises emerged when the researchers, led by Corby Kistler at the University of Minnesota, compared two different strains. There were more than 10,000 differences between the two sequences. Those differences, however, were not spread evenly along the DNA; more than half of the differences were concentrated in just one eighth of the sequence.

So some regions of the genome are much less stable than others. And what genes are in those regions? Mostly ones concerned with infection and virulence, among them the genes for compounds that dissolve the host cell walls and others that digest host molecules so that the fungus can make use of them.

Just why the variability in Fusarium graminearum is concentrated in some areas of the DNA is not yet clear. These areas seem to be hotspots for recombination, which shuffles the DNA during sexual reproduction and so promotes diversity, but this particular fungus doesn’t go in for sexual reproduction all that often. A mystery, then, but one that may still yield new approaches to breeding resistant wheat and barley and perhaps to new kinds of treatment.

You may remember that a joint team of Israeli and US researchers recently reported that a wild relative of wheat, Sharon Goatgrass (Aegilops sharonensis), is loaded with resistance genes that protect it against seven of the most important fungal diseases of wheat. Alas, none of the samples tested was resistant to Fusarium head blight. How about some other wild relative species, though? We shall see.

I say kumato

The FreshPlaza piece on the kumato is not very long. But it does manage to squeeze in a lot of interesting information. The kumato is a tomato that ripens from green to dark brown. It is the result of a conventional breeding programme which involved a wild species. And it is just coming up to its first harvest in Australia. This definitely deserved more investigation.

There’s no doubt it looks pretty extraordinary. But the most intriguing thing about the kumato is that the wild species involved in its development may be from the Galapagos.

Now, Lycopersicon cheesmaniae from the Galapagos Islands has been used to breed dark orange tomatoes before, though it does not have a dark brown skin like the kumato. ((This species was actually published as L. cheesmanii, after Evelyn Cheesman, but that was incorrect, as the Latinists among us will know, as Ms Cheesman was a woman and the specific epithet therefore requires a feminine ending.)) Check out this excerpt from an article celebrating the late great tomato geneticist and explorer Prof. Charles M. Rick in 1997, five years before his death:

Rick’s research led him on 15 genetic scavenger hunts to Andean South America, the homeland of the tomato, where he hunted for wild tomato varieties carrying useful genes. Among his discoveries were wild tomatoes growing near the tidelands of the Galapagos Islands, despite salty sprays that would have stunted or killed a domestic tomato plant.

Or again:

An excellent lecturer, Rick was much sought after by universities who valued both his rigorous science and his humor and flair for storytelling. A perennial favorite involved his frustrations in trying to germinate wild tomato seeds collected from the Galapagos Islands. The emerging mystery of how the plants reproduce in the wild was only resolved after the seeds were “processed” by passing through the digestive track of a Galapagos tortoise, resulting in vigorous seedlings.

The kumato should actually be the Kumato©. It was bred by Syngenta, and first released in the UK in about 2004, I think. But the Roguelands Heirloom Vegetable Seeds Company also has 40 different dark brown to black-skinned varieties in its collection, and says black tomato varieties first appeared in the 19th century in Ukraine.

Screening potatoes for micronutrients

Yet more about iron (and other assorted micronutrients). A recent post of mine elicited a comment from Glenn to the effect that breeders have screened germplasm collections of the major staples for micronutrient composition. I was skeptical about the extent to which this has been done (though not, I must add, about the fact that there will be much more of it in the future). Another post, this one by Jeremy, suggested that there was precious little information out there about variety-level nutritional information.

Well, I’ve now come across a paper that allows us to put some numbers on the amount of screening that has been done for one staple crop, the potato. There’s only an abstract freely available online, but a paper by CIP scientists reports (among other things) on micronutrient levels in native potato varieties in Peru:

Several studies have reported mineral concentrations in improved potatoes… However, limited information was available about the mineral concentration of potato germplasm and breeding materials until 2006. A detailed study was undertaken to determine the levels of Fe and Zn in 37 native varieties, both grown by farmers as well as from the collection under custody at CIP.

The potatoes were grown in a couple of different places. There was lots of variation, both genetic and due to the environment where they were grown, and also an interaction between these factors. And the heritability was high, suggesting that there is potential for improvement through selection and breeding.

But let’s remember that the total CIP potato collection amounts to over 7,500 accessions. That means that some 0.5% has been screened. A good start, but still only a start.

Wheats and gluten

Sometimes it takes some personal connection to get me motivated enough to try and understand something a little more fully. Laziness, I guess. Anyway, for example, I vaguely knew about the gluten seed storage proteins of wheat and the coeliac disease they cause in about 1% of the population. But I decided to delve a little deeper only when an old friend I hadn’t seen for a while visited today and told me that she was a sufferer, and that she needed to know how to describe the condition in italian so she wouldn’t get into trouble eating in restaurants here in Rome.

Having sorted that out, I was interested to know whether there are differences among wheat species in the “toxicity” of their glutens. You’ll remember that wheat comes in a polyploid series: diploid, tetraploids and hexaploids. And that three distinct genomes are involved: AA, BB and DD. Diploid einkorn (AA) and BB genome species got together to form tetraploid emmer and durum wheat (AABB). And these hybridized with wild diploid Triticum tauschii to make hexaploid (AABBDD) bread wheat.

It turns out that differences in gluten toxicity do exist. An analysis of the ancestral A, B and D genomes of wheat found that DNA sequences associated with 4 peptides that have been identified as triggering a response in coeliac patients are not distributed at random. For example, the B genome sequences analyzed did not reveal any of the “guilty” sequences.

On the basis of such insight, breeding strategies can be designed to generate less toxic varieties of wheat which may be tolerated by at least part of the [coelic disease] patient population.

Oh, and coeliac disease is called celiachia in italian.