A schematic representation of the 20E regulated events during the first vitellogenic cycle in the fat body of the mosquito A. aegypti.
After a blood meal activation, a high level of 20E acts via EcRA/USPB heterodimer activating early genes, BrZ2, E74B and E75A, which synergistically activate late genes such as Vg –. TOR, activated by amino acids and insulin, is essential for activating late genes , . TOR is also involved in inhibition of the programmed autophagy during vitellogenesis . HR3 is inhibited by E75A , but activated by EcRA/USPB ensuring its timely expression. At the termination time, lowering of the 20E titer results in repressive action of BriZ1 (not shown) and BrZ4 on late genes such as Vg , . In this study, we have shown that HR3 is involved in inhibition of late target genes expression (Vg). On the other hand, HR3 activates the EcRB/USPA heterodimer. EcR has been shown to repress TOR and activate autophagy . We postulate that it is the EcRB/USPA heterodimer that is responsible for these functions mediating action of HR3; however, this link requires additional confirmation. HR3 acts as an activator of betaFTZ-F1 that in turn is essential for maintaining cyclicity of egg development. The green ovals – EcR/USP 20E heterodimeric receptor; blue boxes – genes that encode 20E regulated transcription factors (early genes); purple boxes – Target-of Rapamycin; black boxes – autophagy; orange boxes – late target genes. Green arrows depict activating effects and red lines - repressive effects. The basics of the scheme were adapted from for comparison reasons.