Abstract
The participation of a divergent mosquito transforming growth factor-β (TGF-β) and mammalian TGF-β1 in the
Anopheles stephensi response to malaria parasite development [Infect. Genet. Evol. 1 (2001) 131–141; Infect. Immun. 71 (2003) 3000–3009] suggests that a network of
Anopheles TGF-β ligands and signaling pathways figure prominently in immune defense of this important vector group. To provide a basis for identifying the roles of these proteins in
Anopheles innate immunity, we identified six predicted TGF-β ligand-encoding genes in the
Anopheles gambiae genome, including two expressed, diverged copies of 60A, the first evidence of ligand gene duplication outside of chordates. In addition to five predicted type I and II receptors, we identified three
Smad genes in the
A. gambiae genome that would be predicted to support both TGF-β/Activin- and bone morphogenetic protein (BMP)-like signaling. All three
Smad genes are expressed in an immunocompetent
A. stephensi cell line and in the
A. stephensi midgut epithelium, confirming that a conserved signaling architecture is in place to support signaling by divergent exogenous and endogenous TGF-β superfamily proteins.