CLL, together with C1qR, suppresses WSSV infection by regulating the activation of Dorsal
Date:2025-10-22 Page Views: 12

Xiao-Tong Cao,Lian-Jie Wu,Jia-Yu Si,Xian-Wei Wang,Jiang-Feng Lan

Abstract

There is no evidence that arthropods possess a complement system. In  arthropods, only gC1qR has been reported. The functional convergence of  gC1qR in arthropods and vertebrates during evolution remains to be  further elucidated. In the present study, a C-type lectin named PcCLL,  which contains a C1q-like sequence (a segment of the C1q globular head)  and might be involved in antiviral immunity, was identified in Procambarus clarkii.  When crayfish are infected with white spot syndrome virus (WSSV), some  C1qRs (gC1qR homologs), which are located at the cell membrane,  recognize WSSV by interacting with the envelope protein VP28.  Subsequently, C1qR recruits PcCLL in the cell, and the C1qR-PcCLL  complexes synergistically promote the nuclear translocation of Dorsal.  Serine-arginine protein kinase (SRPK) is an essential molecule in this  process. The C1qR-PcCLL-SRPK axis regulates the activation and translocation of Dorsal. Finally, the C1qR-PcCLL-Dorsal axis can promote resistance to WSSV infection by regulating the expression of the lectin-like protein (PcLT).  In both vertebrates and arthropods, C1qR appears to participate in  antiviral immunity, but the mechanisms were different. This may  highlight a fascinating evolutionary trajectory across animals.

Paper Linkage:https://doi.org/10.1128/jvi.00416-25

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