Autoimmune response, triggered by genes, can be a barrier to producing a viable offspring

Sep 4 2007

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, they're 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 Weigel's 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 typically be expressed as during immune response following infection, or by autoimmune mutants.

Moreover, further analysis revealed that the parents carried healthy genes; their necrotic offspring were not results of genetic disorders. They were the result of a “bad luck” pairing of genetic variants for genes that are normally used to recognize pathogen attack, Dangl said.

“A normal immune system function can give rise to incompatibility in the next generation,” Dangl said. And if studies move beyond plants, “I predict it will be the same in animals.”

Dangl suggested that the necrotic plant is possibly analogous to a fertilized egg that fails to implant in the uterus. Infertility in couples might be explained by analogous auto-immune genetic profile. “How many couples can't produce progeny, but when they separate and find another mate, they do?”

The study showed “why basic research is so vital,” said Dangl, who was elected into the National Academy of Sciences earlier this year. “This was non-outcome oriented research. If we had set out to study hybrid reproduction we would not have found this fascinating system.”