Article

Functional regulatory divergence of the innate immune system in interspecific Drosophila hybrids.

Field of Genetics and Development, Department of Molecular Biology and Genetics, Cornell University.
Molecular Biology and Evolution (impact factor: 5.55). 11/2010; 27(11):2596-605. DOI:10.1093/molbev/msq146 pp.2596-605
Source: PubMed

ABSTRACT In order to investigate divergence of immune regulation among Drosophila species, we have engaged in a study of innate immune function in F1 hybrids of Drosophila melanogaster and D. simulans. If pathways have diverged between the species such that incompatibilities have arisen between interacting components of the immune network, we expect the hybrids to display dysregulation of immune genes. We have quantified gene induction in hybrid and parental flies in response to bacterial infection. These results show that although the hybrids do not suffer widespread immune breakdown, they show significantly different regulation of many immune genes relative to the parents. We examine this divergence in terms of additivity and expression differences among genes, observing distinct patterns of dysregulation among functional groups within the pathways of the innate immune system. The functional groups most sensitive to misexpression in the hybrids are the downstream components of the network, indicative of some propagation of dysregulation throughout the immune pathways. Interestingly, this dysregulation does not appear to associate with phenotypic differences in bacterial load after infection in hybrids, possibly highlighting some robustness of function of the innate immune response to perturbations like hybridization.

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Keywords

bacterial infection
 
bacterial load
 
D. simulans
 
display dysregulation
 
distinct patterns
 
divergence
 
downstream components
 
Drosophila species
 
expression differences
 
F1 hybrids
 
functional groups
 
immune genes
 
immune network
 
immune pathways
 
immune regulation
 
innate immune function
 
innate immune response
 
innate immune system
 
interacting components
 
widespread immune breakdown
 

Erin M Hill-Burns