|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|||||||
|
|
||||||||||
|
|
|
|
|
|
|
|
|
|||
 |
|
|
|
|
 |
|
|||
|
|
|||
|
 |
September 4, 2007 In the latest issue of PLoS Biology, CCGS/Biology professor Jeff Dangl and his collaborator Detlef Weigel at the Max Planck Institute describe a new connection between autoimmunity and hybrid necrosis that creates barriers to the flow of genetic transmission within a plant species. Using the model plant Arabidopsis thaliana, the researchers crossed 280 genetically distinct strains and found that about 2% of their 881 unique progeny displayed hybrid necrosis with a similar suite of phenotypic properties, suggesting a common underlying mechanism. In many cases, they found that this underlying mechanism was the activation of an autoimmune-like response in the progeny similar to what is seen when an otherwise healthy plant is infected by a pathogen. They noted that the hybrid necrosis was nearly always di-genic, consistent with the classical Dobzhansky-Muller model for speciation. The genes responsible for hybrid necrosis apparently confer a selective advantage for the parents in warding off infection, but can prove fatal for their progeny in certain unfortunate combinations. Because the autoimmune syndrome they studied is widespread in both intra- and inter-specific crosses in plant kingdom, Dangl and Weigel suggest that this genetic tradeoff between having an effective immune system at the expense of reproductive compatibility might be the first step toward speciation and the evolution of gene-flow barriers in plants. Research article in PLoS Biology
|
|
|
|
|
|||