Analysis of Schistosoma mansoni genes shared with Deuterostomia and with possible roles in host interactions

dc.contributor.authorVenancio, Thiago M.en
dc.contributor.authorDeMarco, Ricardoen
dc.contributor.authorAlmeida, Giulliana T.en
dc.contributor.authorOliveira, Katia C.en
dc.contributor.authorSetubal, João C.en
dc.contributor.authorVerjovski-Almeida, Sergioen
dc.date.accessioned2012-08-24T12:08:53Zen
dc.date.available2012-08-24T12:08:53Zen
dc.date.issued2007-11-08en
dc.date.updated2012-08-24T12:08:53Zen
dc.description.abstractBackground: Schistosoma 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. Results: In 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. Conclusion: The 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.en
dc.description.versionPublished versionen
dc.format.mimetypeapplication/pdfen
dc.identifier.citationBMC Genomics. 2007 Nov 08;8(1):407en
dc.identifier.doihttps://doi.org/10.1186/1471-2164-8-407en
dc.identifier.urihttp://hdl.handle.net/10919/18914en
dc.language.isoenen
dc.rightsCreative Commons Attribution 4.0 Internationalen
dc.rights.holderThiago M Venancio et al.; licensee BioMed Central Ltd.en
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/en
dc.titleAnalysis of Schistosoma mansoni genes shared with Deuterostomia and with possible roles in host interactionsen
dc.title.serialBMC Genomicsen
dc.typeArticle - Refereeden
dc.type.dcmitypeTexten

Files

Original bundle
Now showing 1 - 5 of 6
Name:
1471-2164-8-407.xml
Size:
147.34 KB
Format:
Extensible Markup Language
Loading...
Thumbnail Image
Name:
1471-2164-8-407.pdf
Size:
1.4 MB
Format:
Adobe Portable Document Format
Loading...
Thumbnail Image
Name:
1471-2164-8-407-S4.PDF
Size:
67.47 KB
Format:
Adobe Portable Document Format
Loading...
Thumbnail Image
Name:
1471-2164-8-407-S3.PDF
Size:
270.03 KB
Format:
Adobe Portable Document Format
Name:
1471-2164-8-407-S2.XLS
Size:
108 KB
Format:
Microsoft Excel
License bundle
Now showing 1 - 1 of 1
Name:
license.txt
Size:
1.5 KB
Format:
Item-specific license agreed upon to submission
Description: