ArticleBMC genomics2007
Analysis of Schistosoma mansoni genes shared with Deuterostomia and with possible roles in host interactions.
Article in BMC genomics, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 13 citations in OpenAlex.
- Discovery of Schistosoma mekongi circulating proteins and antigens in infected mouse sera.PloS one · 2022Article
- Adults from Kisumu, Kenya have robust γδ T cell responses to Schistosoma mansoni, which are modulated by tuberculosis.PLoS neglected tropical diseases · 2020Article
- Gamma delta T cells in non-immune patients during primary schistosomal infection.Immunity, inflammation and disease · 2014Article
- The IRF family of transcription factors: Inception, impact and implications in oncogenesis.Oncoimmunology · 2012Article
- Proteolytically Derived Endogenous Angioinhibitors Originating from the Extracellular Matrix.Pharmaceuticals (Basel, Switzerland) · 2011Article
- Survey of transcripts expressed by the invasive juvenile stage of the liver fluke Fasciola hepatica.BMC genomics · 2010Article
- The Vasohibin Family.Pharmaceuticals (Basel, Switzerland) · 2010Review
- Dynamic evolution of immune system regulators: the history of the interferon regulatory factor family.Molecular biology and evolution · 2009Article
- Discovery of multiple neuropeptide families in the phylum Platyhelminthes.International journal for parasitology · 2009Article
- Schistosoma mansoni tegument protein Sm29 is able to induce a Th1-type of immune response and protection against parasite infection.PLoS neglected tropical diseases · 2008Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSchistosoma mansoni is a blood helminth parasite that causes schistosomiasis, a disease that affects 200 million people in the world. Many orthologs of known mammalian genes have been discovered in this parasite and evidence is accumulating that some of these genes encode proteins linked to signaling pathways in the parasite that appear to be involved with growth or development, suggesting a complex co-evolutionary process.
resultsIn this work we found 427 genes conserved in the Deuterostomia group that have orthologs in S. mansoni and no members in any nematodes and insects so far sequenced. Among these genes we have identified Insulin Induced Gene (INSIG), Interferon Regulatory Factor (IRF) and vasohibin orthologs, known to be involved in mammals in mevalonate metabolism, immune response and angiogenesis control, respectively. We have chosen these three genes for a more detailed characterization, which included extension of their cloned messages to obtain full-length sequences. Interestingly, SmINSIG showed a 10-fold higher expression in adult females as opposed to males, in accordance with its possible role in regulating egg production. SmIRF has a DNA binding domain, a tryptophan-rich N-terminal region and several predicted phosphorylation sites, usually important for IRF activity. Fourteen different alternatively spliced forms of the S. mansoni vasohibin (SmVASL) gene were detected that encode seven different protein isoforms including one with a complete C-terminal end, and other isoforms with shorter C-terminal portions. Using S. mansoni homologs, we have employed a parsimonious rationale to compute the total gene losses/gains in nematodes, arthropods and deuterostomes under either the Coelomata or the Ecdysozoa evolutionary hypotheses; our results show a lower losses/gains number under the latter hypothesis.
conclusionThe genes discussed which are conserved between S. mansoni and deuterostomes, probably have an ancient origin and were lost in Ecdysozoa, being still present in Lophotrochozoa. Given their known functions in Deuterostomia, it is possible that some of them have been co-opted to perform functions related (directly or indirectly) to host adaptation or interaction with host signaling processes.
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