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?).

Backyard domestication

There’s a “dump heap” hypothesis of agricultural origins which suggests that people first got interested in actively managing and manipulating plants for food or other products when they saw them sprouting out of piles of garbage in and about settlements. There they could observe them daily and experiment with them. A slight variation on this theme — involving corrals in pastoralist campsites rather than garbage dumps — has been proposed for the domestication of quinoa.

One of the things that might have happened in these fertile micro-environments in close proximity to human habitations is that different related species might have been brought accidentally together, leading to hybridization and the development of interesting new — polyploid — types. But there really hasn’t been much empirical evidence for this.

No more. A new paper ((Colin E. Hughes, Rajanikanth Govindarajulu, Ashley Robertson, Denis L. Filer, Stephen A. Harris, and C. Donovan Bailey. Serendipitous backyard hybridization and the origin of crops. PNAS published August 17, 2007, 10.1073/pnas.0702193104.)) looks at the domestication of the legume tree Leucaena in Mexico, where it is grown for food (it is also used as a fodder in some parts of the world). A variety of evidence is discussed which suggests that there has indeed been much hybridization among up to 13 different wild species of Leucaena in Mexican backyards. This has proved “a potent trigger for domestication.” The authors think a similar thing also happened in Mexico with two other perennial crops, Agave and Opuntia.

Rusty conclusions about iron deficiency

Iron deficiency anaemia is a big problem. WHO estimates that about 2 billion people — that’s roughly one in three — lack enough iron in the diet. And the consequences are grave for health and the economies of developing countries. So of course people are focused on ways to combat iron deficiency. Two hog the limelight: supplementation by adding iron to the diet and biofortification, breeding to add more iron to the staples that make up the diet. A recent paper in The Lancet reviews the story of iron deficiency and how to treat it. ((Michael B Zimmermann and Richard F Hurrell, Nutritional iron deficiency, The Lancet, 370 (9586), 11 August 2007-17 August 2007, Pp 511-520.)) Perhaps not surprisingly, the study concludes that “targeted iron supplementation, iron fortification of foods, or both, can control iron deficiency in populations”. And yet, having said that “dietary iron bioavailability is low in populations consuming monotonous plant-based diets,” the authors do not appear to have seriously considered the idea of trying to attack that monotony instead. Maybe enriching and diversifying those plant-based diets to include more dark green leafy vegetables and more pulses would be as effective, with additional benefits in other realms. But that kind of intervention isn’t nearly as glamorous, and gets little attention.

Of course, it could be that solving the problem of iron deficiency will just give rise to other difficulties. Another paper suggests that iron deficiency protects us against some of the epidemic contagious diseases that have hitched along as people crowded together in agriculturally-fed cities. ((S Denic and M Agarwal, Nutritional iron deficiency: an evolutionary perspective. Nutrition. 2007, 23:603-14. Epub 2007 Jun 20.)) Maybe iron deficiency — at least in moderation — is a good thing?

A second helping of rice

More today to satisfy your hunger for rice information, hot on the heels of the recent paper trying to explain the pattern of genetic variation across and within two subspecies of cultivated rice, discussed by Jeremy a couple of days ago.

First there’s a paper ((Global Dissemination of a Single Mutation Conferring White Pericarp in Rice. Sweeney MT, Thomson MJ, Cho YG, Park YJ, Williamson SH, et al. PLoS Genetics Vol. 3, No. 8.)) looking at how the red pericarp of wild rice became the white pericarp of cultivated rice. The answer is that a mutation arose in the japonica subspecies, crossed to the indica and became fixed in both under very strong selection pressure by ancient rice farmers. They must have really liked those funny mutant white grains when they first noticed them! Oh to have been a fly on the wall — or a brown plant hopper on the rice stalk — when the white pericarp mutation was first noticed in some ancient paddy…

Then comes news that the three CGIAR centres with an interest in rice — IRRI, WARDA and CIAT — are to boost their collaboration to solve the pressing production problems of Africa. There’s talk of forming a consortium. More flags being prepared.