BACKGROUND Calcineurin is involved in numerous of cellular processes and Ca2+-dependent signal transduction pathways. With thousands of host larval (Spodoptera exigua) transcripts are downregulated after the infection of Heliothis virescens… Click to show full abstract
BACKGROUND Calcineurin is involved in numerous of cellular processes and Ca2+-dependent signal transduction pathways. With thousands of host larval (Spodoptera exigua) transcripts are downregulated after the infection of Heliothis virescens ascovirus 3h (HvAV-3h) in our previous transcriptome studies, the calcineurin encoded genes (SeCaNs) were highly upregulated. To understand the regulation of SeCaNs in S. exigua larvae during the infection of HvAV-3h, the function of calcineurin subunit A (SeCaN-SubA) and calcineurin binding protein (SeCaN-BP) were analyzed. RESULTS The in vitro assays indicated that the bacterial expressed PrSeCaN-SubA was an acid phosphatase, but no phosphatase activity was detected with the purified PrSeCaN-BP. The transcription level of SeCaN-SubA was upregulated after HvAV-3h infection and the calcineurin activity was significantly increased after HvAV-3h infection in S. exigua larvae. Interestingly, the SeCaN-BP transcripts were only detectable in the HvAV-3h infected larvae. Further immunoblotting results consistently agree with those obtained by qPCR which indicate that the infection of HvAV-3h caused the upregulated expression of SeCaN-SubA and the appearance of SeCaN-BP. An interaction between the cleaved SeCaN-SubA and SeCaN-BP was detected by co immunoprecipitation assays, and the expression of SeCaN-BP in Sf9 cells can help to increase the calcineurin activity of SeCaN-SubA. Further investigations with CaN inhibitors suggested that HvAV-3h stimulates host larval CaN activity enhance viral replication. CONCLUSION The increase of calcineurin activity caused by HvAV-3h infection might be due to the upregulation of SeCaN-SubA and the induced expression of SeCaN-BP, and the increased calcineurin activity is essential for the ascoviral replication. This article is protected by copyright. All rights reserved.
               
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