Characterisation and functional role of a novel C1qDC protein from a colonial ascidian
As an invertebrate, the compound ascidian Botryllus schlosseri faces nonself only with innate immunity. In this species, we already identified the key components of the lectin and alternative complement activation pathways. In the present work, by mining the transcriptome, we identified a single tra...
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Published in | Developmental and comparative immunology Vol. 122; p. 104077 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
United States
Elsevier Ltd
01.09.2021
Elsevier Science Ltd |
Subjects | |
Online Access | Get full text |
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Summary: | As an invertebrate, the compound ascidian Botryllus schlosseri faces nonself only with innate immunity. In this species, we already identified the key components of the lectin and alternative complement activation pathways. In the present work, by mining the transcriptome, we identified a single transcript codifying for a protein, member of the C1q-domain-containing protein family, with a signal peptide followed by two globular C1q (gC1q) domains. It shares a similar domain organisation with C1q/TNF-related proteins 4, the only vertebrate protein family with two gC1q domains. Our gC1q domain-containing protein, called BsC1qDC, is actively transcribed by immunocytes. The transcription is modulated during the Botryllus blastogenetic cycle and is upregulated following the injection of Bacillus clausii cells in the circulation. Furthermore, the injection of bsc1qdc iRNA in the vasculature results in decreased transcription of the gene and a significant impairment of phagocytosis and degranulation, suggesting the involvement of this molecule in immune responses.
•BsC1qDC is a novel C1q domain-containing protein in Botryllus schlosseri.•It is transcribed by circulating immunocytes.•Its transcription is modulated during the colonial blastogenetic cycle.•BsC1qDC transcription is upregulated in the presence of nonself.•BsC1dDC is involved in phagocytosis and the triggering of inflammation. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0145-305X 1879-0089 |
DOI: | 10.1016/j.dci.2021.104077 |