sRNAs as possible regulators of retrotransposon activity in Cryptococcus gattii VGII

Detalhes bibliográficos
Autor(a) principal: Ferrarese, Patricia Aline Grös
Data de Publicação: 2017
Outros Autores: Streit, Rodrigo Silva Araujo, Santos, Francine Melise dos, Schrank, Augusto, Silva, Lívia Kmetzsch Rosa e
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Repositório Institucional da UFRGS
Texto Completo: http://hdl.handle.net/10183/221827
Resumo: Background: The absence of Argonaute genes in the fungal pathogen Cryptococcus gattii R265 and other VGII strains indicates that yeasts of this genotype cannot have a functional RNAi pathway, an evolutionarily conserved gene silencing mechanism performed by small RNAs. The success of the R265 strain as a pathogen that caused the Pacific Northwest and Vancouver Island outbreaks may imply that RNAi machinery loss could be beneficial under certain circumstances during evolution. As a result, a hypermutant phenotype would be created with high rates of genome retrotransposition, for instance. This study therefore aimed to evaluate in silicio the effect of retrotransposons and their control mechanisms by small RNAs on genomic stability and synteny loss of C. gattii R265 through retrotransposons sequence comparison and orthology analysis with other 16 C. gattii genomic sequences available. Results: Retrotransposon mining identified a higher sequence count to VGI genotype compared to VGII, VGIII, and VGIV. However, despite the lower retrotransposon number, VGII exhibited increased synteny loss and genome rearrangement events. RNA-Seq analysis indicated highly expressed retrotransposons as well as sRNA production. Conclusions: Genome rearrangement and synteny loss may suggest a greater retrotransposon mobilization caused by RNAi pathway absence, but the effective presence of sRNAs that matches retrotransposon sequences means that an alternative retrotransposon silencing mechanism could be active in genomic integrity maintenance of C. gattii VGII strains.
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spelling Ferrarese, Patricia Aline GrösStreit, Rodrigo Silva AraujoSantos, Francine Melise dosSchrank, AugustoSilva, Lívia Kmetzsch Rosa e2021-06-02T04:34:02Z20171471-2164http://hdl.handle.net/10183/221827001072349Background: The absence of Argonaute genes in the fungal pathogen Cryptococcus gattii R265 and other VGII strains indicates that yeasts of this genotype cannot have a functional RNAi pathway, an evolutionarily conserved gene silencing mechanism performed by small RNAs. The success of the R265 strain as a pathogen that caused the Pacific Northwest and Vancouver Island outbreaks may imply that RNAi machinery loss could be beneficial under certain circumstances during evolution. As a result, a hypermutant phenotype would be created with high rates of genome retrotransposition, for instance. This study therefore aimed to evaluate in silicio the effect of retrotransposons and their control mechanisms by small RNAs on genomic stability and synteny loss of C. gattii R265 through retrotransposons sequence comparison and orthology analysis with other 16 C. gattii genomic sequences available. Results: Retrotransposon mining identified a higher sequence count to VGI genotype compared to VGII, VGIII, and VGIV. However, despite the lower retrotransposon number, VGII exhibited increased synteny loss and genome rearrangement events. RNA-Seq analysis indicated highly expressed retrotransposons as well as sRNA production. Conclusions: Genome rearrangement and synteny loss may suggest a greater retrotransposon mobilization caused by RNAi pathway absence, but the effective presence of sRNAs that matches retrotransposon sequences means that an alternative retrotransposon silencing mechanism could be active in genomic integrity maintenance of C. gattii VGII strains.application/pdfengBMC Genomics. London. Vol. 18, No. 294, (2017), p. 1-14Cryptococcus gattiiRNAiRetrotransposonsSyntenysRNAs as possible regulators of retrotransposon activity in Cryptococcus gattii VGIIEstrangeiroinfo:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da UFRGSinstname:Universidade Federal do Rio Grande do Sul (UFRGS)instacron:UFRGSTEXT001072349.pdf.txt001072349.pdf.txtExtracted Texttext/plain65370http://www.lume.ufrgs.br/bitstream/10183/221827/2/001072349.pdf.txt1ee7f9868d216eeb1433948394c4f906MD52ORIGINAL001072349.pdfTexto completo (inglês)application/pdf1258449http://www.lume.ufrgs.br/bitstream/10183/221827/1/001072349.pdf75e3039dedd46d8a3b6d7af7b5553d09MD5110183/2218272023-07-06 03:53:48.319519oai:www.lume.ufrgs.br:10183/221827Repositório de PublicaçõesPUBhttps://lume.ufrgs.br/oai/requestopendoar:2023-07-06T06:53:48Repositório Institucional da UFRGS - Universidade Federal do Rio Grande do Sul (UFRGS)false
dc.title.pt_BR.fl_str_mv sRNAs as possible regulators of retrotransposon activity in Cryptococcus gattii VGII
title sRNAs as possible regulators of retrotransposon activity in Cryptococcus gattii VGII
spellingShingle sRNAs as possible regulators of retrotransposon activity in Cryptococcus gattii VGII
Ferrarese, Patricia Aline Grös
Cryptococcus gattii
RNAi
Retrotransposons
Synteny
title_short sRNAs as possible regulators of retrotransposon activity in Cryptococcus gattii VGII
title_full sRNAs as possible regulators of retrotransposon activity in Cryptococcus gattii VGII
title_fullStr sRNAs as possible regulators of retrotransposon activity in Cryptococcus gattii VGII
title_full_unstemmed sRNAs as possible regulators of retrotransposon activity in Cryptococcus gattii VGII
title_sort sRNAs as possible regulators of retrotransposon activity in Cryptococcus gattii VGII
author Ferrarese, Patricia Aline Grös
author_facet Ferrarese, Patricia Aline Grös
Streit, Rodrigo Silva Araujo
Santos, Francine Melise dos
Schrank, Augusto
Silva, Lívia Kmetzsch Rosa e
author_role author
author2 Streit, Rodrigo Silva Araujo
Santos, Francine Melise dos
Schrank, Augusto
Silva, Lívia Kmetzsch Rosa e
author2_role author
author
author
author
dc.contributor.author.fl_str_mv Ferrarese, Patricia Aline Grös
Streit, Rodrigo Silva Araujo
Santos, Francine Melise dos
Schrank, Augusto
Silva, Lívia Kmetzsch Rosa e
dc.subject.por.fl_str_mv Cryptococcus gattii
RNAi
topic Cryptococcus gattii
RNAi
Retrotransposons
Synteny
dc.subject.eng.fl_str_mv Retrotransposons
Synteny
description Background: The absence of Argonaute genes in the fungal pathogen Cryptococcus gattii R265 and other VGII strains indicates that yeasts of this genotype cannot have a functional RNAi pathway, an evolutionarily conserved gene silencing mechanism performed by small RNAs. The success of the R265 strain as a pathogen that caused the Pacific Northwest and Vancouver Island outbreaks may imply that RNAi machinery loss could be beneficial under certain circumstances during evolution. As a result, a hypermutant phenotype would be created with high rates of genome retrotransposition, for instance. This study therefore aimed to evaluate in silicio the effect of retrotransposons and their control mechanisms by small RNAs on genomic stability and synteny loss of C. gattii R265 through retrotransposons sequence comparison and orthology analysis with other 16 C. gattii genomic sequences available. Results: Retrotransposon mining identified a higher sequence count to VGI genotype compared to VGII, VGIII, and VGIV. However, despite the lower retrotransposon number, VGII exhibited increased synteny loss and genome rearrangement events. RNA-Seq analysis indicated highly expressed retrotransposons as well as sRNA production. Conclusions: Genome rearrangement and synteny loss may suggest a greater retrotransposon mobilization caused by RNAi pathway absence, but the effective presence of sRNAs that matches retrotransposon sequences means that an alternative retrotransposon silencing mechanism could be active in genomic integrity maintenance of C. gattii VGII strains.
publishDate 2017
dc.date.issued.fl_str_mv 2017
dc.date.accessioned.fl_str_mv 2021-06-02T04:34:02Z
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dc.identifier.issn.pt_BR.fl_str_mv 1471-2164
dc.identifier.nrb.pt_BR.fl_str_mv 001072349
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dc.language.iso.fl_str_mv eng
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dc.relation.ispartof.pt_BR.fl_str_mv BMC Genomics. London. Vol. 18, No. 294, (2017), p. 1-14
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