Efeito do nocaute da mitofusina 2 sobre a mitocôndria, o retículo endoplasmático e a mitofagia em oócitos murinos
Ano de defesa: | 2018 |
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Autor(a) principal: | |
Orientador(a): | |
Banca de defesa: | |
Tipo de documento: | Dissertação |
Tipo de acesso: | Acesso aberto |
Idioma: | por |
Instituição de defesa: |
Universidade Federal de São Carlos
Câmpus São Carlos |
Programa de Pós-Graduação: |
Programa de Pós-Graduação em Genética Evolutiva e Biologia Molecular - PPGGEv
|
Departamento: |
Não Informado pela instituição
|
País: |
Não Informado pela instituição
|
Palavras-chave em Português: | |
Palavras-chave em Inglês: | |
Área do conhecimento CNPq: | |
Link de acesso: | https://repositorio.ufscar.br/handle/ufscar/10613 |
Resumo: | Mitofusins 1 (MFN1) and 2 (MFN2) are transmembrane GTPases present in the outer mitochondrial membrane and involved in the regulation of mitochondrial fusion. Since MFN2 is also present in the membrane of the endoplasmic reticulum (ER), it is also responsible for regulating the morphology and its interaction with the mitochondria. Thus, there is increasing evidence that MFN2 plays a key role in the regulation of mitochondrial function and ER, as well as the autophagic pathway. However, little is known about its role in the oocyte. Recently, we have observed that the conditional knockout of Mfn2 in murine oocytes (Mfn2-null) does not significantly alter fertility, but results in hyperglycemia in the offspring. Therefore, the objective of this work was to investigate the molecular mechanisms that result in these phenotypes. The effects of the conditional knockout of Mfn2 on the oocyte were evaluated considering the function of mitochondria, RE and the occurrence of mitofagia. For this, we first confirmed the effects of the conditional knockout of Mfn2. Knockout oocytes for Mfn2 were able to develop normally when matured in vitro. Pups from knockout oocytes showed alterations in blood glucose levels in the tests of glucose intolerance and insulin resistance when compared to wild-type oocyte (WT) pups. In addition, we found alterations in mitochondria of oocyte knockout regarding number (WT = 0.061 ± 0.004 and Mfn2-null = 0.037 ± 0.003 organelle / μm2), crests morphology, area (WT = 0.589 ± 0.015 and Mfn2-null = 1.673 ± 0.101 μm2) and contact with RE. However, Mfn2 knockout resulted in decreased lipid content in ovulated oocytes (WT = 13.07 ± 0.96 and Mfn2-null = 9.65 ± 0.64 % of lipid-occupied area of ooplasm). In addition, no evidence was found at the transcriptional level of ER stress. As regards mitophagy, no knockout effect of Mfn2 was observed on the expression of genes involved in this pathway, as well as on co-localization between mitochondria and autophagosomes (WT = 0.65 ± 0.05 and Mfn2-null = 0.53 ± 0.04 AU). Thus, these findings demonstrate that conditional knockout of Mfn2 in the oocyte results in metabolic changes in offspring, most likely due to changes in morphology, function and contact between mitochondria and ER. However, the molecular mechanism by which this occurs still lacks elucidation. Furthermore, we have demonstrated that conditional knockout of Mfn2 can be a good model for the study of the inheritance of metabolic syndromes. |
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Garcia, Bruna MartinsChiaratti, Marcos Robertohttp://lattes.cnpq.br/0392078007500289http://lattes.cnpq.br/90314231115501282018-10-24T20:17:00Z2018-10-24T20:17:00Z2018-08-24GARCIA, Bruna Martins. Efeito do nocaute da mitofusina 2 sobre a mitocôndria, o retículo endoplasmático e a mitofagia em oócitos murinos. 2018. Dissertação (Mestrado em Genética Evolutiva e Biologia Molecular) – Universidade Federal de São Carlos, São Carlos, 2018. Disponível em: https://repositorio.ufscar.br/handle/ufscar/10613.https://repositorio.ufscar.br/handle/ufscar/10613Mitofusins 1 (MFN1) and 2 (MFN2) are transmembrane GTPases present in the outer mitochondrial membrane and involved in the regulation of mitochondrial fusion. Since MFN2 is also present in the membrane of the endoplasmic reticulum (ER), it is also responsible for regulating the morphology and its interaction with the mitochondria. Thus, there is increasing evidence that MFN2 plays a key role in the regulation of mitochondrial function and ER, as well as the autophagic pathway. However, little is known about its role in the oocyte. Recently, we have observed that the conditional knockout of Mfn2 in murine oocytes (Mfn2-null) does not significantly alter fertility, but results in hyperglycemia in the offspring. Therefore, the objective of this work was to investigate the molecular mechanisms that result in these phenotypes. The effects of the conditional knockout of Mfn2 on the oocyte were evaluated considering the function of mitochondria, RE and the occurrence of mitofagia. For this, we first confirmed the effects of the conditional knockout of Mfn2. Knockout oocytes for Mfn2 were able to develop normally when matured in vitro. Pups from knockout oocytes showed alterations in blood glucose levels in the tests of glucose intolerance and insulin resistance when compared to wild-type oocyte (WT) pups. In addition, we found alterations in mitochondria of oocyte knockout regarding number (WT = 0.061 ± 0.004 and Mfn2-null = 0.037 ± 0.003 organelle / μm2), crests morphology, area (WT = 0.589 ± 0.015 and Mfn2-null = 1.673 ± 0.101 μm2) and contact with RE. However, Mfn2 knockout resulted in decreased lipid content in ovulated oocytes (WT = 13.07 ± 0.96 and Mfn2-null = 9.65 ± 0.64 % of lipid-occupied area of ooplasm). In addition, no evidence was found at the transcriptional level of ER stress. As regards mitophagy, no knockout effect of Mfn2 was observed on the expression of genes involved in this pathway, as well as on co-localization between mitochondria and autophagosomes (WT = 0.65 ± 0.05 and Mfn2-null = 0.53 ± 0.04 AU). Thus, these findings demonstrate that conditional knockout of Mfn2 in the oocyte results in metabolic changes in offspring, most likely due to changes in morphology, function and contact between mitochondria and ER. However, the molecular mechanism by which this occurs still lacks elucidation. Furthermore, we have demonstrated that conditional knockout of Mfn2 can be a good model for the study of the inheritance of metabolic syndromes.As mitofusinas 1 (MFN1) e 2 (MFN2) são GTPases transmembranares presentes na membrana mitocondrial externa e envolvidas na regulação da fusão mitocondrial. Uma vez que o MFN2 também está presente na membrana do retículo endoplasmático (RE), ele também é responsável por regular a morfologia e a interação deste com a mitocôndria. Assim, são crescentes as evidências de que o MFN2 desempenha um papel chave na regulação da função mitocondrial e do RE, assim como, da via autofágica. Todavia, pouco se sabe sobre a sua função no oócito. Recentemente, observamos que o knockout condicional do Mfn2 em oócitos murinos (Mfn2-null) não altera significantemente a fertilidade, mas resulta em hiperglicemia na prole. Sendo assim, o objetivo deste trabalho foi investigar os mecanismos moleculares que resultam nesses fenótipos. Os efeitos do knockout condicional do Mfn2 no oócito foram avaliados considerando a função da mitocôndria, do RE e a ocorrência de mitofagia. Para isso, primeiramente confirmamos os efeitos do knockout condicional do Mfn2. Oócitos knockout para Mfn2 foram capazes de se desenvolver normalmente quando maturados in vitro. Já os filhotes oriundos de oócitos knockout demostraram alterações nos níveis de glicose sanguínea nos testes de intolerância a glicose e resistência a insulina quando comparados com os filhotes oriundos de oócitos selvagens (WT). Além disso, encontramos nas mitocôndrias de oócitos knockout alterações de número (WT = 0,061 ± 0,004 e Mfn2-null = 0,037 ± 0,003 organela/µm2), morfologia das cristas, área (WT = 0,589 ± 0,015 e Mfn2-null = 1,673 ± 0,101 µm2) e contato com o RE. Todavia, o knockout do Mfn2 resultou em diminuição do conteúdo lipídico em oócitos ovulados (WT = 13,07 ± 0,96 e Mfn2-null = 9,65 ± 0,64% de área de ooplasma ocupada por lipídeos). Ademais, não foi encontrado indícios a nível transcricional de estresse do RE. No que diz respeito a mitofagia, não foi encontrado efeito do knockout do Mfn2 sobre a expressão de genes participantes dessa via, assim como sobre a co-localização entre mitocôndrias e autofagossomos (WT = 0,65 ± 0,05 e Mfn2-null = 0,53 ± 0,04 U.A). Sendo assim, esses achados demonstram que o knockout condicional do Mfn2 no oócito resulta em alterações metabólicas na prole devido, muito provavelmente, as alterações na morfologia, função e contato entre mitocôndria e RE. Todavia, o mecanismo molecular pelo qual isso ocorre ainda carece de elucidação. Ainda, demonstramos que o knockout condicional do Mfn2 pode vir a ser um bom modelo para o estudo da herança de síndromes metabólicas.Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)CAPES: Código de Financiamento 001FAPESP: 2016/11935-9FAPESP: 2012/50231-6FAPESP: 2017/05899-2porUniversidade Federal de São CarlosCâmpus São CarlosPrograma de Pós-Graduação em Genética Evolutiva e Biologia Molecular - PPGGEvUFSCarOócitoMitofusina 2MitocôndriaRetículo endoplasmáticoSíndrome metabólicaOocyteMitofusin 2MitochondriaEndoplasmic reticulumMetabolic syndromeCIENCIAS BIOLOGICAS::BIOQUIMICA::BIOLOGIA MOLECULAREfeito do nocaute da mitofusina 2 sobre a mitocôndria, o retículo endoplasmático e a mitofagia em oócitos murinosEffect of mitofusin 2 knockout on mitochondria, endoplasmic reticulum and mitofagia in murine oocytesinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/masterThesisOnlineinfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da UFSCARinstname:Universidade Federal de São Carlos (UFSCAR)instacron:UFSCARORIGINALdissertação final.pdfdissertação final.pdfapplication/pdf8662853https://{{ getenv "DSPACE_HOST" "repositorio.ufscar.br" }}/bitstream/ufscar/10613/1/dissertac%cc%a7a%cc%83o%20final.pdf1e004c32c9c5aba32ac74d8aa2981cb3MD51LICENSElicense.txtlicense.txttext/plain; charset=utf-81957https://{{ getenv "DSPACE_HOST" "repositorio.ufscar.br" }}/bitstream/ufscar/10613/4/license.txtae0398b6f8b235e40ad82cba6c50031dMD54TEXTdissertação final.pdf.txtdissertação final.pdf.txtExtracted texttext/plain160808https://{{ getenv "DSPACE_HOST" "repositorio.ufscar.br" }}/bitstream/ufscar/10613/5/dissertac%cc%a7a%cc%83o%20final.pdf.txt9984bb428174b952ca2924240e79c759MD55THUMBNAILdissertação final.pdf.jpgdissertação final.pdf.jpgIM Thumbnailimage/jpeg5531https://{{ getenv "DSPACE_HOST" "repositorio.ufscar.br" }}/bitstream/ufscar/10613/6/dissertac%cc%a7a%cc%83o%20final.pdf.jpg8d8e2914d67d829036df62a87d11673aMD56ufscar/106132019-09-11 03:24:51.002oai:repositorio.ufscar.br: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Repositório InstitucionalPUBhttps://repositorio.ufscar.br/oai/requestopendoar:43222023-05-25T12:56:38.652680Repositório Institucional da UFSCAR - Universidade Federal de São Carlos (UFSCAR)false |
dc.title.por.fl_str_mv |
Efeito do nocaute da mitofusina 2 sobre a mitocôndria, o retículo endoplasmático e a mitofagia em oócitos murinos |
dc.title.alternative.eng.fl_str_mv |
Effect of mitofusin 2 knockout on mitochondria, endoplasmic reticulum and mitofagia in murine oocytes |
title |
Efeito do nocaute da mitofusina 2 sobre a mitocôndria, o retículo endoplasmático e a mitofagia em oócitos murinos |
spellingShingle |
Efeito do nocaute da mitofusina 2 sobre a mitocôndria, o retículo endoplasmático e a mitofagia em oócitos murinos Garcia, Bruna Martins Oócito Mitofusina 2 Mitocôndria Retículo endoplasmático Síndrome metabólica Oocyte Mitofusin 2 Mitochondria Endoplasmic reticulum Metabolic syndrome CIENCIAS BIOLOGICAS::BIOQUIMICA::BIOLOGIA MOLECULAR |
title_short |
Efeito do nocaute da mitofusina 2 sobre a mitocôndria, o retículo endoplasmático e a mitofagia em oócitos murinos |
title_full |
Efeito do nocaute da mitofusina 2 sobre a mitocôndria, o retículo endoplasmático e a mitofagia em oócitos murinos |
title_fullStr |
Efeito do nocaute da mitofusina 2 sobre a mitocôndria, o retículo endoplasmático e a mitofagia em oócitos murinos |
title_full_unstemmed |
Efeito do nocaute da mitofusina 2 sobre a mitocôndria, o retículo endoplasmático e a mitofagia em oócitos murinos |
title_sort |
Efeito do nocaute da mitofusina 2 sobre a mitocôndria, o retículo endoplasmático e a mitofagia em oócitos murinos |
author |
Garcia, Bruna Martins |
author_facet |
Garcia, Bruna Martins |
author_role |
author |
dc.contributor.authorlattes.por.fl_str_mv |
http://lattes.cnpq.br/9031423111550128 |
dc.contributor.author.fl_str_mv |
Garcia, Bruna Martins |
dc.contributor.advisor1.fl_str_mv |
Chiaratti, Marcos Roberto |
dc.contributor.advisor1Lattes.fl_str_mv |
http://lattes.cnpq.br/0392078007500289 |
contributor_str_mv |
Chiaratti, Marcos Roberto |
dc.subject.por.fl_str_mv |
Oócito Mitofusina 2 Mitocôndria Retículo endoplasmático Síndrome metabólica |
topic |
Oócito Mitofusina 2 Mitocôndria Retículo endoplasmático Síndrome metabólica Oocyte Mitofusin 2 Mitochondria Endoplasmic reticulum Metabolic syndrome CIENCIAS BIOLOGICAS::BIOQUIMICA::BIOLOGIA MOLECULAR |
dc.subject.eng.fl_str_mv |
Oocyte Mitofusin 2 Mitochondria Endoplasmic reticulum Metabolic syndrome |
dc.subject.cnpq.fl_str_mv |
CIENCIAS BIOLOGICAS::BIOQUIMICA::BIOLOGIA MOLECULAR |
description |
Mitofusins 1 (MFN1) and 2 (MFN2) are transmembrane GTPases present in the outer mitochondrial membrane and involved in the regulation of mitochondrial fusion. Since MFN2 is also present in the membrane of the endoplasmic reticulum (ER), it is also responsible for regulating the morphology and its interaction with the mitochondria. Thus, there is increasing evidence that MFN2 plays a key role in the regulation of mitochondrial function and ER, as well as the autophagic pathway. However, little is known about its role in the oocyte. Recently, we have observed that the conditional knockout of Mfn2 in murine oocytes (Mfn2-null) does not significantly alter fertility, but results in hyperglycemia in the offspring. Therefore, the objective of this work was to investigate the molecular mechanisms that result in these phenotypes. The effects of the conditional knockout of Mfn2 on the oocyte were evaluated considering the function of mitochondria, RE and the occurrence of mitofagia. For this, we first confirmed the effects of the conditional knockout of Mfn2. Knockout oocytes for Mfn2 were able to develop normally when matured in vitro. Pups from knockout oocytes showed alterations in blood glucose levels in the tests of glucose intolerance and insulin resistance when compared to wild-type oocyte (WT) pups. In addition, we found alterations in mitochondria of oocyte knockout regarding number (WT = 0.061 ± 0.004 and Mfn2-null = 0.037 ± 0.003 organelle / μm2), crests morphology, area (WT = 0.589 ± 0.015 and Mfn2-null = 1.673 ± 0.101 μm2) and contact with RE. However, Mfn2 knockout resulted in decreased lipid content in ovulated oocytes (WT = 13.07 ± 0.96 and Mfn2-null = 9.65 ± 0.64 % of lipid-occupied area of ooplasm). In addition, no evidence was found at the transcriptional level of ER stress. As regards mitophagy, no knockout effect of Mfn2 was observed on the expression of genes involved in this pathway, as well as on co-localization between mitochondria and autophagosomes (WT = 0.65 ± 0.05 and Mfn2-null = 0.53 ± 0.04 AU). Thus, these findings demonstrate that conditional knockout of Mfn2 in the oocyte results in metabolic changes in offspring, most likely due to changes in morphology, function and contact between mitochondria and ER. However, the molecular mechanism by which this occurs still lacks elucidation. Furthermore, we have demonstrated that conditional knockout of Mfn2 can be a good model for the study of the inheritance of metabolic syndromes. |
publishDate |
2018 |
dc.date.accessioned.fl_str_mv |
2018-10-24T20:17:00Z |
dc.date.available.fl_str_mv |
2018-10-24T20:17:00Z |
dc.date.issued.fl_str_mv |
2018-08-24 |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/masterThesis |
format |
masterThesis |
status_str |
publishedVersion |
dc.identifier.citation.fl_str_mv |
GARCIA, Bruna Martins. Efeito do nocaute da mitofusina 2 sobre a mitocôndria, o retículo endoplasmático e a mitofagia em oócitos murinos. 2018. Dissertação (Mestrado em Genética Evolutiva e Biologia Molecular) – Universidade Federal de São Carlos, São Carlos, 2018. Disponível em: https://repositorio.ufscar.br/handle/ufscar/10613. |
dc.identifier.uri.fl_str_mv |
https://repositorio.ufscar.br/handle/ufscar/10613 |
identifier_str_mv |
GARCIA, Bruna Martins. Efeito do nocaute da mitofusina 2 sobre a mitocôndria, o retículo endoplasmático e a mitofagia em oócitos murinos. 2018. Dissertação (Mestrado em Genética Evolutiva e Biologia Molecular) – Universidade Federal de São Carlos, São Carlos, 2018. Disponível em: https://repositorio.ufscar.br/handle/ufscar/10613. |
url |
https://repositorio.ufscar.br/handle/ufscar/10613 |
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Universidade Federal de São Carlos Câmpus São Carlos |
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Programa de Pós-Graduação em Genética Evolutiva e Biologia Molecular - PPGGEv |
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UFSCar |
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Universidade Federal de São Carlos Câmpus São Carlos |
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