Differential expression profiles of miRNAs and their putative targets in Schistosoma mansoni during its life cycle.

BACKGROUND: Schistosomiasis is a disease caused by Schistosoma. Due to its complex life cycle, evolutionary position and sexual dimorphism, schistosomes have several mechanisms of gene regulation. MicroRNAs (miRNAs) are short endogenous RNAs that regulate gene expression at the post-transcriptional level by targeting mRNA transcripts. OBJECTIVES: Here, we tested 12 miRNAs and identified their putative targets using a computational approach. METHODS: We performed the expression profiles of a set of miRNAs and their putative targets during the parasite's life cycle by quantitative reverse transcription-polymerase chain reaction (qRT-PCR). FINDINGS: Our results showed differential expression patterns of the mature miRNAs sma-miR-250; sma-miR-92a; sma-miR-new_4-3p; sma-miR-new_4-5p; sma-miR-new_5-5p; sma-miR-new_12-5p; sma-miR-new_13-3p and sma-miR-new_13-5p. Interestingly, many of the putative target genes are linked to oxidative phosphorylation and are up-regulated in adult-worms, which led us to suggest that miRNAs might play important roles in the post-transcriptional regulation of genes related to energetic metabolism inversion during parasite development. It is noteworthy that the expression of sma-miR-new_13-3p exhibited a negative correlation on SmNADH:ubiquinone oxidoreductase complex I. MAIN CONCLUSIONS: Our analysis revealed putative miRNA genes related to important biological processes, such as transforming growth factor beta (TGF-ß) signaling, proteasome regulation, glucose and lipid metabolism, immune system evasion and transcriptional regulation.

Detection of Schistosoma mansoni long non-coding RNAs in the infected C57BL/6 mouse liver.

Long non-coding RNAs (lncRNAs) perform several types of regulatory functions and have been recently explored in the genus Schistosoma. Although sequencing and bioinformatics approaches have demonstrated the presence of hundreds of lncRNAs and microRNAs (miRNAs) in this genus, information regarding their abundance, characteristics, and potential functions linked to Schistosoma mansoni biology and parasite-host interaction is limited. Our objectives in the present study were to verify whether 15 previously identified S. mansoni lncRNAs are detectable in the host liver. In addition, we assess whether these lncRNAs are present in the S. mansoni infective form and the stages inside the definitive host. The detection of these 15 S. mansoni lncRNAs and a long terminal repeat (LTR) retrotransposon Saci 4 was performed in the eggs, cercariae, and 3.5-h schistosomula. All lncRNAs were found to be expressed in these stages; some of the lncRNAs were found in the livers of the infected C57BL/6 mice. In conclusion, S. mansoni lncRNAs were detected in host livers and quantified. Furthermore, many of the lncRNAs analyzed showed differential expression in the larval stages, indicating that they play a stage-specific regulatory role.

Differential expression profiles of miRNAs and their putative targets in Schistosoma mansoni during its life cycle

BACKGROUND Schistosomiasis is a disease caused by Schistosoma. Due to its complex life cycle, evolutionary position and sexual dimorphism, schistosomes have several mechanisms of gene regulation. MicroRNAs (miRNAs) are short endogenous RNAs that regulate gene expression at the post-transcriptional level by targeting mRNA transcripts. OBJECTIVES Here, we tested 12 miRNAs and identified their putative targets using a computational approach. METHODS We performed the expression profiles of a set of miRNAs and their putative targets during the parasite's life cycle by quantitative reverse transcription-polymerase chain reaction (qRT-PCR). FINDINGS Our results showed differential expression patterns of the mature miRNAs sma-miR-250; sma-miR-92a; sma-miR-new_4-3p; sma-miR-new_4-5p; sma-miR-new_5-5p; sma-miR-new_12-5p; sma-miR-new_13-3p and sma-miR-new_13-5p. Interestingly, many of the putative target genes are linked to oxidative phosphorylation and are up-regulated in adult-worms, which led us to suggest that miRNAs might play important roles in the post-transcriptional regulation of genes related to energetic metabolism inversion during parasite development. It is noteworthy that the expression of sma-miR-new_13-3p exhibited a negative correlation on SmNADH:ubiquinone oxidoreductase complex I. MAIN CONCLUSIONS Our analysis revealed putative miRNA genes related to important biological processes, such as transforming growth factor beta (TGF-β) signaling, proteasome regulation, glucose and lipid metabolism, immune system evasion and transcriptional regulation.

Manganese (II) removal from aqueous solutions by Cladosporium halotolerans and Hypocrea jecorina.

Manganese (Mn) is toxic at higher concentrations requiring its removal before returning the wastewater to the environment. This article reported the Mn removal of two fungi strains isolated from mine wastewater. ITS rRNA region sequencing identified the fungi strains as Cladosporium halotolerans and Hypocrea jecorina. Mn2+ removal assays were performed in Sabouraud broth with 50 mg L-1 Mn2+ supplemented and bioleaching assays using MnO2 instead of MnSO4 at the same conditions. C. halotolerans removed 96 % of 50 mg L-1 Mn2+ at two weeks without MnO2 bioleaching with 649.9 mg of biomass and H. jecorina removed about 50 % of Mn2+ in 21 days from initial 50 mg of Mn2+ L-1 with 316.8 mg of biomass. Extracellular laccases were present in C. halotolerans agar regardless of the Mn addition. Mn adsorbed was detected on C. halotolerans hyphae. Mn oxidation was positive to H. jecorina by reaction of its medium with Leucoberbelin blue.

Epigenetic and parasitological parameters are modulated in EBi3-/- mice infected with Schistosoma mansoni.

Schistosoma mansoni adaptive success is related to regulation of replication, transcription and translation inside and outside the intermediate and definitive host. We hypothesize that S. mansoni alters its epigenetic state in response to the mammalian host immune system, reprogramming gene expression and altering the number of eggs. In response, a change in the DNA methylation profile of hepatocytes could occurs, modulating the extent of hepatic granuloma. To investigate this hypothesis, we used the EBi3-/- murine (Mus musculus) model of S. mansoni infection and evaluated changes in new and maintenance DNA methylation profiles in the liver after 55 days of infection. We evaluated expression of epigenetic genes and genes linked to histone deubiquitination in male and female S. mansoni worms. Comparing TET expression with DNMT expression indicated that DNA demethylation exceeds methylation in knockout infected and uninfected mice and in wild-type infected and uninfected mice. S. mansoni infection provokes activation of demethylation in EBi3-/-I mice (knockout infected). EBi3-/-C (knockout uninfected) mice present intrinsically higher DNA methylation than WTC (control uninfected) mice. EBi3-/-I mice show decreased hepatic damage considering volume and reduced number of granulomas compared to WTI mice; the absence of IL27 and IL35 pathways decreases the Th1 response resulting in minor liver damage. S. mansoni males and females recovered from EBi3-/-I mice have reduced expression of a deubiquitinating enzyme gene, orthologs of which target histones and affect chromatin state. SmMBD and SmHDAC1 expression levels are downregulated in male and female parasites recovered from EBi3-/-, leading to epigenetic gene downregulation in S. mansoni. Changes to the immunological background thus induce epigenetic changes in hepatic tissues and alterations in S. mansoni gene expression, which attenuate liver symptoms in the acute phase of schistosomiasis.