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 1.

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.

Pigs didn’t fly, walked to Europe

We know that agriculture began in the Fertile Crescent about 12,000 years ago and then spread across Europe between 9,000 and 6,000 years ago. But what exactly was it that spread? Was it the idea of agriculture or agriculturalists themselves? Just-published work on the DNA of modern and ancient pigs says it was probably a bit of both. It seems that Middle Eastern farmers migrated into Europe carrying their agrobiodiversity with them — crops and domesticated animals. But, as far as the pig was concerned anyway, they soon adopted a locally domesticated version in preference to the Middle Eastern type they had brought along.

In vino veritas

Thanks to Ola Westengen for contributing this post.

Serendipity seems to be the modus operandi of this great blog and so is the case with this post. On a trip last Sunday to look at this Etruscan world heritage site outside Cerveteri I stumbled into a Sagra dell’Uva –a town festival to celebrate the grape. I took the picture shown below and had some great Cerveteri Bianco Secco before walking on to the amazing Etruscan ruins. Then back in the office I came across a news item from the latest edition of Nature about the newly published sequence of the grapevine genome. The French-Italian consortium of researchers has read the half billion letter book of life of the variety Pinot Noir.

The draft sequence of the grapevine genome is the fourth one produced so far for flowering plants, the second for a woody species and the first for a fruit crop. Grapevine was selected because of its important place in the cultural heritage of humanity beginning during the Neolithic period.

grapes.JPG

The authors cite the Greek historian Thucydides, who wrote that Mediterranean people began to emerge from ignorance when they learnt to cultivate olives and grapes. I’m still ignorant, but it is starting to dawn on me that vine buffs must be some of the best perpetuators and celebrators of agricultural biodiversity — just take a look at the variety list on Wikipedia.

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.

Fido decoded

An article by Elaine Ostrander in the latest American Scientist summarizes recent advances in canine genomics, which have been considerable:

The dog genome has been mapped and sequenced. A host of disease loci have been mapped, and in many cases the underlying mutations identified. Our understanding of how dog breeds relate to one another is beginning to develop, and we have a fundamental understanding of the organization of the canine genome. The issue of complex traits is no longer off-limits. We have begun to understand the genetic portfolio that leads to variation in body size and shape, and even some performance-associated behaviors.

Some snippets:

  1. Between-breed genetic variation is about 27.5% of the total, compared to about 5% between human populations.
  2. Dog breeds fall into 4 main groups: Asian and African dogs, plus grey wolves; mastiffs; herding dogs and sight hounds; and modern huntings dogs.
  3. 75% of the 19,000 genes that have been identified in the dog genome show close similarities with their human counterparts.
  4. Variation in a single gene (IGF1) explains a lot of the size differences among and within breeds.

What to do with all this information?

It is certainly hoped that the disease-gene mapping will lead to the production of genetic tests and more thoughtful breeding programs associated with healthier, more long-lived dogs. It will be easier to select for particular physical traits such as body size or coat color… Finally, canine geneticists will have a chance to develop an understanding of the genes that cause breed-specific behaviors (why do pointers point and herders herd?).