Auto immune response creates barrier to fertility; could be a step in ...( Plant biologists at the Max Planck I...)

Plant biologists at the Max Planck Institute of Developmental Biology and the University of North Carolina at Chapel Hill have discovered that an autoimmune response, triggered by a small number of genes, can be a barrier to producing a viable offspring.

Studying Arabidopsis thaliana, sometimes called thale cress, the researchers identified a phenotype that, when paired together from a male and female, produced plants that survived only long enough to produce a few leaves, then died a phenomenon called hybrid necrosis; literally, death. The dead plants resembled what would result from a mortal infection, despite the absence of a pathogen.

This finding presents a new theory in the development of new species: two plants of the same species fail to reproduce not because of infestation or infection from an outside organism, nor from problems with reproductive organs.

If two otherwise healthy members of a species cannot produce progeny, theyre on a track toward no longer being members of the same species, said Jeff Dangl, Ph.D., John N. Couch professor of biology, microbiology and immunology and associate director of the Carolina Center for Genome Sciences. This could be a very early event in what will, over time, lead to speciation.

The study appears in the Sept. 4, 2007, issue of PLoS Biology.

The initial finding was serendipitous, Dangl said. Detlef Weigel, at Max Planck, shared with Dangl some photos of Arabidopsis hybrids from a project by Kirsten Bomblies, a postdoctoral fellow in Weigels lab that was meant to study the timing of flowering..

I said, those look just like autoimmune mutants, Dangl recalled.

Bomblies, Weigel and others at Max Planck crossed 280 genetically different strains of Arabidopsis from around the world into 881 different combinations: 2 percent of these crosses gave necrotic offspring. They all had similar gene expression profiles, a group of about 1,000 genes that would
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