Slc25a36 modulates pluripotency of mouse embryonic stem cells by regulating mitochondrial function and glutathione level
Mitochondria play a central role in the maintenance of the naive state of embryonic stem cells. Many details of the mechanism remain to be fully elucidated. Solute carrier family 25 member 36 ( ) might regulate mitochondrial function through transporting pyrimidine nucleotides for mtDNA/RNA synthesi...
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| Veröffentlicht in: | Biochemical journal 2019-06, Vol.476 (11), p.1585-1604 |
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| creator | Xin, Yanli Wang, Yanliang Zhong, Liang Shi, Bingbo Liang, Hui Han, Jianyong |
| description | Mitochondria play a central role in the maintenance of the naive state of embryonic stem cells. Many details of the mechanism remain to be fully elucidated. Solute carrier family 25 member 36 (
) might regulate mitochondrial function through transporting pyrimidine nucleotides for mtDNA/RNA synthesis. Its physical role in this process remains unknown; however,
was recently found to be highly expressed in naive mouse embryonic stem cells (mESCs). Here, the function of
was characterized as a maintenance factor of mESCs pluripotency.
deficiency (via knockdown) has been demonstrated to result in mitochondrial dysfunction, which induces the differentiation of mESCs. The expression of key pluripotency markers (
,
,
, and
) decreased, while that of key TE genes (
,
, and
) increased.
-positive cells emerged in
6-deficient colonies under trophoblast stem cell culture conditions. As a result of
6 deficiency, mtDNA of knockdown cells declined, leading to impaired mitochondria with swollen morphology, decreased mitochondrial membrane potential, and low numbers. The key transcription regulators of mitochondrial biogenesis also decreased. These results indicate that mitochondrial dysfunction leads to an inability to support the pluripotency maintenance. Moreover, down-regulated glutathione metabolism and up-regulated focal adhesion reinforced and stabilized the process of differentiation by separately enhancing OCT4 degradation and promoting cell spread. This study improves the understanding of the function of
, as well as the relationship of mitochondrial function with naive pluripotency maintenance and stem cell fate decision. |
| doi_str_mv | 10.1042/BCJ20190057 |
| format | Article |
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) might regulate mitochondrial function through transporting pyrimidine nucleotides for mtDNA/RNA synthesis. Its physical role in this process remains unknown; however,
was recently found to be highly expressed in naive mouse embryonic stem cells (mESCs). Here, the function of
was characterized as a maintenance factor of mESCs pluripotency.
deficiency (via knockdown) has been demonstrated to result in mitochondrial dysfunction, which induces the differentiation of mESCs. The expression of key pluripotency markers (
,
,
, and
) decreased, while that of key TE genes (
,
, and
) increased.
-positive cells emerged in
6-deficient colonies under trophoblast stem cell culture conditions. As a result of
6 deficiency, mtDNA of knockdown cells declined, leading to impaired mitochondria with swollen morphology, decreased mitochondrial membrane potential, and low numbers. The key transcription regulators of mitochondrial biogenesis also decreased. These results indicate that mitochondrial dysfunction leads to an inability to support the pluripotency maintenance. Moreover, down-regulated glutathione metabolism and up-regulated focal adhesion reinforced and stabilized the process of differentiation by separately enhancing OCT4 degradation and promoting cell spread. This study improves the understanding of the function of
, as well as the relationship of mitochondrial function with naive pluripotency maintenance and stem cell fate decision.</description><identifier>ISSN: 0264-6021</identifier><identifier>EISSN: 1470-8728</identifier><identifier>DOI: 10.1042/BCJ20190057</identifier><identifier>PMID: 31036718</identifier><language>eng</language><publisher>England</publisher><subject>Animals ; CDX2 Transcription Factor - metabolism ; Cell Differentiation - genetics ; Cells, Cultured ; DNA, Mitochondrial - genetics ; DNA, Mitochondrial - metabolism ; Focal Adhesions ; Gene Expression Regulation ; Gene Knockdown Techniques ; Glutathione - metabolism ; Mice ; Mitochondria - metabolism ; Mitochondria - ultrastructure ; Mitochondrial Membrane Transport Proteins - antagonists & inhibitors ; Mitochondrial Membrane Transport Proteins - genetics ; Mitochondrial Membrane Transport Proteins - metabolism ; Mitochondrial Proteins - antagonists & inhibitors ; Mitochondrial Proteins - genetics ; Mitochondrial Proteins - metabolism ; Mouse Embryonic Stem Cells - cytology ; Mouse Embryonic Stem Cells - metabolism ; Nucleotide Transport Proteins - antagonists & inhibitors ; Nucleotide Transport Proteins - genetics ; Nucleotide Transport Proteins - metabolism ; Octamer Transcription Factor-3 - metabolism</subject><ispartof>Biochemical journal, 2019-06, Vol.476 (11), p.1585-1604</ispartof><rights>2019 The Author(s). Published by Portland Press Limited on behalf of the Biochemical Society.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c289t-aa78495e1f044ea6809ffa09f23d22ea1890f44e9715f17d6eae849cd3adcdbb3</citedby><cites>FETCH-LOGICAL-c289t-aa78495e1f044ea6809ffa09f23d22ea1890f44e9715f17d6eae849cd3adcdbb3</cites><orcidid>0000-0002-9549-3279</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,3252,27903,27904</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31036718$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Xin, Yanli</creatorcontrib><creatorcontrib>Wang, Yanliang</creatorcontrib><creatorcontrib>Zhong, Liang</creatorcontrib><creatorcontrib>Shi, Bingbo</creatorcontrib><creatorcontrib>Liang, Hui</creatorcontrib><creatorcontrib>Han, Jianyong</creatorcontrib><title>Slc25a36 modulates pluripotency of mouse embryonic stem cells by regulating mitochondrial function and glutathione level</title><title>Biochemical journal</title><addtitle>Biochem J</addtitle><description>Mitochondria play a central role in the maintenance of the naive state of embryonic stem cells. Many details of the mechanism remain to be fully elucidated. Solute carrier family 25 member 36 (
) might regulate mitochondrial function through transporting pyrimidine nucleotides for mtDNA/RNA synthesis. Its physical role in this process remains unknown; however,
was recently found to be highly expressed in naive mouse embryonic stem cells (mESCs). Here, the function of
was characterized as a maintenance factor of mESCs pluripotency.
deficiency (via knockdown) has been demonstrated to result in mitochondrial dysfunction, which induces the differentiation of mESCs. The expression of key pluripotency markers (
,
,
, and
) decreased, while that of key TE genes (
,
, and
) increased.
-positive cells emerged in
6-deficient colonies under trophoblast stem cell culture conditions. As a result of
6 deficiency, mtDNA of knockdown cells declined, leading to impaired mitochondria with swollen morphology, decreased mitochondrial membrane potential, and low numbers. The key transcription regulators of mitochondrial biogenesis also decreased. These results indicate that mitochondrial dysfunction leads to an inability to support the pluripotency maintenance. Moreover, down-regulated glutathione metabolism and up-regulated focal adhesion reinforced and stabilized the process of differentiation by separately enhancing OCT4 degradation and promoting cell spread. This study improves the understanding of the function of
, as well as the relationship of mitochondrial function with naive pluripotency maintenance and stem cell fate decision.</description><subject>Animals</subject><subject>CDX2 Transcription Factor - metabolism</subject><subject>Cell Differentiation - genetics</subject><subject>Cells, Cultured</subject><subject>DNA, Mitochondrial - genetics</subject><subject>DNA, Mitochondrial - metabolism</subject><subject>Focal Adhesions</subject><subject>Gene Expression Regulation</subject><subject>Gene Knockdown Techniques</subject><subject>Glutathione - metabolism</subject><subject>Mice</subject><subject>Mitochondria - metabolism</subject><subject>Mitochondria - ultrastructure</subject><subject>Mitochondrial Membrane Transport Proteins - antagonists & inhibitors</subject><subject>Mitochondrial Membrane Transport Proteins - genetics</subject><subject>Mitochondrial Membrane Transport Proteins - metabolism</subject><subject>Mitochondrial Proteins - antagonists & inhibitors</subject><subject>Mitochondrial Proteins - genetics</subject><subject>Mitochondrial Proteins - metabolism</subject><subject>Mouse Embryonic Stem Cells - cytology</subject><subject>Mouse Embryonic Stem Cells - metabolism</subject><subject>Nucleotide Transport Proteins - antagonists & inhibitors</subject><subject>Nucleotide Transport Proteins - genetics</subject><subject>Nucleotide Transport Proteins - metabolism</subject><subject>Octamer Transcription Factor-3 - metabolism</subject><issn>0264-6021</issn><issn>1470-8728</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpNkM1LxDAQxYMoun6cvEuOglQnadq0R138RPCgnkuaTNZK2qxJKu5_b5dV8TLD8H5vmHmEHDM4ZyD4xdX8gQOrAQq5RWZMSMgqyattMgNeiqwEzvbIfozvAEyAgF2ylzPIS8mqGfl6dpoXKi9p783oVMJIl24M3dInHPSKejspY0SKfRtWfug0jQl7qtG5SNsVDbhY-7phQfsuef3mBxM65agdB506P1A1GLpwY1LpbRqROvxEd0h2rHIRj376AXm9uX6Z32WPT7f388vHTPOqTplSshJ1gcyCEKjKCmpr1VR4bjhHxaoa7KTUkhWWSVOiwsmgTa6MNm2bH5DTzd5l8B8jxtT0XVwfrwac_mo4Z1JIVhZyQs82qA4-xoC2WYauV2HVMGjWUTf_op7ok5_FY9uj-WN_s82_AcBne4c</recordid><startdate>20190614</startdate><enddate>20190614</enddate><creator>Xin, Yanli</creator><creator>Wang, Yanliang</creator><creator>Zhong, Liang</creator><creator>Shi, Bingbo</creator><creator>Liang, Hui</creator><creator>Han, Jianyong</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-9549-3279</orcidid></search><sort><creationdate>20190614</creationdate><title>Slc25a36 modulates pluripotency of mouse embryonic stem cells by regulating mitochondrial function and glutathione level</title><author>Xin, Yanli ; Wang, Yanliang ; Zhong, Liang ; Shi, Bingbo ; Liang, Hui ; Han, Jianyong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c289t-aa78495e1f044ea6809ffa09f23d22ea1890f44e9715f17d6eae849cd3adcdbb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Animals</topic><topic>CDX2 Transcription Factor - metabolism</topic><topic>Cell Differentiation - genetics</topic><topic>Cells, Cultured</topic><topic>DNA, Mitochondrial - genetics</topic><topic>DNA, Mitochondrial - metabolism</topic><topic>Focal Adhesions</topic><topic>Gene Expression Regulation</topic><topic>Gene Knockdown Techniques</topic><topic>Glutathione - metabolism</topic><topic>Mice</topic><topic>Mitochondria - metabolism</topic><topic>Mitochondria - ultrastructure</topic><topic>Mitochondrial Membrane Transport Proteins - antagonists & inhibitors</topic><topic>Mitochondrial Membrane Transport Proteins - genetics</topic><topic>Mitochondrial Membrane Transport Proteins - metabolism</topic><topic>Mitochondrial Proteins - antagonists & inhibitors</topic><topic>Mitochondrial Proteins - genetics</topic><topic>Mitochondrial Proteins - metabolism</topic><topic>Mouse Embryonic Stem Cells - cytology</topic><topic>Mouse Embryonic Stem Cells - metabolism</topic><topic>Nucleotide Transport Proteins - antagonists & inhibitors</topic><topic>Nucleotide Transport Proteins - genetics</topic><topic>Nucleotide Transport Proteins - metabolism</topic><topic>Octamer Transcription Factor-3 - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Xin, Yanli</creatorcontrib><creatorcontrib>Wang, Yanliang</creatorcontrib><creatorcontrib>Zhong, Liang</creatorcontrib><creatorcontrib>Shi, Bingbo</creatorcontrib><creatorcontrib>Liang, Hui</creatorcontrib><creatorcontrib>Han, Jianyong</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Biochemical journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Xin, Yanli</au><au>Wang, Yanliang</au><au>Zhong, Liang</au><au>Shi, Bingbo</au><au>Liang, Hui</au><au>Han, Jianyong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Slc25a36 modulates pluripotency of mouse embryonic stem cells by regulating mitochondrial function and glutathione level</atitle><jtitle>Biochemical journal</jtitle><addtitle>Biochem J</addtitle><date>2019-06-14</date><risdate>2019</risdate><volume>476</volume><issue>11</issue><spage>1585</spage><epage>1604</epage><pages>1585-1604</pages><issn>0264-6021</issn><eissn>1470-8728</eissn><abstract>Mitochondria play a central role in the maintenance of the naive state of embryonic stem cells. Many details of the mechanism remain to be fully elucidated. Solute carrier family 25 member 36 (
) might regulate mitochondrial function through transporting pyrimidine nucleotides for mtDNA/RNA synthesis. Its physical role in this process remains unknown; however,
was recently found to be highly expressed in naive mouse embryonic stem cells (mESCs). Here, the function of
was characterized as a maintenance factor of mESCs pluripotency.
deficiency (via knockdown) has been demonstrated to result in mitochondrial dysfunction, which induces the differentiation of mESCs. The expression of key pluripotency markers (
,
,
, and
) decreased, while that of key TE genes (
,
, and
) increased.
-positive cells emerged in
6-deficient colonies under trophoblast stem cell culture conditions. As a result of
6 deficiency, mtDNA of knockdown cells declined, leading to impaired mitochondria with swollen morphology, decreased mitochondrial membrane potential, and low numbers. The key transcription regulators of mitochondrial biogenesis also decreased. These results indicate that mitochondrial dysfunction leads to an inability to support the pluripotency maintenance. Moreover, down-regulated glutathione metabolism and up-regulated focal adhesion reinforced and stabilized the process of differentiation by separately enhancing OCT4 degradation and promoting cell spread. This study improves the understanding of the function of
, as well as the relationship of mitochondrial function with naive pluripotency maintenance and stem cell fate decision.</abstract><cop>England</cop><pmid>31036718</pmid><doi>10.1042/BCJ20190057</doi><tpages>20</tpages><orcidid>https://orcid.org/0000-0002-9549-3279</orcidid></addata></record> |
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| source | MEDLINE; Portland Press Electronic Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central |
| subjects | Animals CDX2 Transcription Factor - metabolism Cell Differentiation - genetics Cells, Cultured DNA, Mitochondrial - genetics DNA, Mitochondrial - metabolism Focal Adhesions Gene Expression Regulation Gene Knockdown Techniques Glutathione - metabolism Mice Mitochondria - metabolism Mitochondria - ultrastructure Mitochondrial Membrane Transport Proteins - antagonists & inhibitors Mitochondrial Membrane Transport Proteins - genetics Mitochondrial Membrane Transport Proteins - metabolism Mitochondrial Proteins - antagonists & inhibitors Mitochondrial Proteins - genetics Mitochondrial Proteins - metabolism Mouse Embryonic Stem Cells - cytology Mouse Embryonic Stem Cells - metabolism Nucleotide Transport Proteins - antagonists & inhibitors Nucleotide Transport Proteins - genetics Nucleotide Transport Proteins - metabolism Octamer Transcription Factor-3 - metabolism |
| title | Slc25a36 modulates pluripotency of mouse embryonic stem cells by regulating mitochondrial function and glutathione level |
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