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.
Original language | English (US) |
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Pages (from-to) | 965-977 |
Number of pages | 13 |
Journal | Molecular Immunology |
Volume | 41 |
Issue number | 10 |
DOIs | |
State | Published - Aug 2004 |
Externally published | Yes |
Keywords
- A. stephensi 60A
- ActAR
- ActIIR
- activin A receptor
- activin Type II receptor
- activin-like kinase 2 receptor
- activin-like protein on 23B
- Ag60A
- ALK2R
- ALP23B
- Anopheles
- Anopheles gambiae 60A
- As60A
- Babo
- Baboon
- Immunity
- Malaria
- Mosquito
- Plasmodium
- TGF-β
ASJC Scopus subject areas
- Molecular Biology
- Immunology