Recombinant Bursicon (r-Bursicon) in Aedes aegypti consists of two subunits, burs-α and burs-β, which form heterodimers or homodimers (α-α, β-β) when expressed in heterologous systems like E. coli or insect cells . The heterodimer is the active form responsible for cuticle tanning and wing maturation, while homodimers mediate immune responses .
| Subunit | Molecular Weight | Function |
|---|---|---|
| burs-α | ~15 kDa | Cuticle tanning, wing expansion |
| burs-β | ~13 kDa | Homodimer signaling for immunity |
Heterodimer (α-β): Triggers cuticle sclerotization and melanization after ecdysis, reducing desiccation and providing structural support .
Homodimers (α-α, β-β): Regulate midgut stem cell proliferation and energy homeostasis, as shown in Drosophila melanogaster .
Homodimers (β-β): Induce prophylactic immunity by upregulating antimicrobial peptides (AMPs) such as Cecropin A (CecA), Defensin A (DefA), and Dptericin (Dpt) via the Relish2 transcription factor .
Heterodimer (α-β): May also contribute to AMP expression, though homodimers are more potent .
| AMP Gene | Expression Fold-Change (vs. Control) | Target Pathogens |
|---|---|---|
| CecA | 12.3 ± 1.5 | Gram-negative bacteria |
| DefA | 8.7 ± 0.9 | Gram-positive bacteria |
| Dpt | 6.2 ± 0.8 | Fungi |
Gram-negative (E. coli): 72% growth inhibition (50 μM CecA/DefA) .
Gram-positive (S. aureus): 65% growth inhibition (50 μM DefA) .
Immune Priming: r-Bursicon homodimers (β-β) enhance mosquito resistance to pathogens, potentially reducing disease transmission (e.g., dengue, Zika) .
Genetic Engineering: Overexpression of bursicon homodimers in Aedes aegypti could create disease-resistant mosquito populations .