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In vitro cellular reprogramming to model gonad development and its disorders
During embryonic development, mutually antagonistic signaling cascades determine gonadal fate toward a testicular or ovarian identity. Errors in this process result in disorders of sex development (DSDs), characterized by discordance between chromosomal, gonadal, and anatomical sex. The absence of a...
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| Published in: | Science advances 2023-01, Vol.9 (1), p.eabn9793-eabn9793 |
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| creator | Gonen, Nitzan Eozenou, Caroline Mitter, Richard Elzaiat, Maëva Stévant, Isabelle Aviram, Rona Bernardo, Andreia Sofia Chervova, Almira Wankanit, Somboon Frachon, Emmanuel Commère, Pierre-Henri Brailly-Tabard, Sylvie Valon, Léo Barrio Cano, Laura Levayer, Romain Mazen, Inas Gobaa, Samy Smith, James C McElreavey, Kenneth Lovell-Badge, Robin Bashamboo, Anu |
| description | During embryonic development, mutually antagonistic signaling cascades determine gonadal fate toward a testicular or ovarian identity. Errors in this process result in disorders of sex development (DSDs), characterized by discordance between chromosomal, gonadal, and anatomical sex. The absence of an appropriate, accessible in vitro system is a major obstacle in understanding mechanisms of sex-determination/DSDs. Here, we describe protocols for differentiation of mouse and human pluripotent cells toward gonadal progenitors. Transcriptomic analysis reveals that the in vitro-derived murine gonadal cells are equivalent to embryonic day 11.5 in vivo progenitors. Using similar conditions, Sertoli-like cells derived from 46,XY human induced pluripotent stem cells (hiPSCs) exhibit sustained expression of testis-specific genes, secrete anti-Müllerian hormone, migrate, and form tubular structures. Cells derived from 46,XY DSD female hiPSCs, carrying an
variant, show aberrant gene expression and absence of tubule formation. CRISPR-Cas9-mediated variant correction rescued the phenotype. This is a robust tool to understand mechanisms of sex determination and model DSDs. |
| doi_str_mv | 10.1126/sciadv.abn9793 |
| format | article |
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variant, show aberrant gene expression and absence of tubule formation. CRISPR-Cas9-mediated variant correction rescued the phenotype. This is a robust tool to understand mechanisms of sex determination and model DSDs.</description><identifier>ISSN: 2375-2548</identifier><identifier>EISSN: 2375-2548</identifier><identifier>DOI: 10.1126/sciadv.abn9793</identifier><identifier>PMID: 36598988</identifier><language>eng</language><publisher>United States: American Association for the Advancement of Science (AAAS)</publisher><subject>Animals ; Biomedicine and Life Sciences ; Cellular Reprogramming ; Cellular Reprogramming - genetics ; Developmental Biology ; Diseases and Disorders ; Female ; Gonadal Dysgenesis, 46,XY ; Gonadal Dysgenesis, 46,XY - genetics ; Gonads ; Humans ; Induced Pluripotent Stem Cells ; Life Sciences ; Male ; Mice ; SciAdv r-articles</subject><ispartof>Science advances, 2023-01, Vol.9 (1), p.eabn9793-eabn9793</ispartof><rights>Attribution</rights><rights>Copyright © 2023 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works. Distributed under a Creative Commons Attribution License 4.0 (CC BY). 2023 The Authors</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c490t-4f447677bbc4d5da6bc342cb3a26073002b60c91c0657ecf14120725ac3509ba3</citedby><cites>FETCH-LOGICAL-c490t-4f447677bbc4d5da6bc342cb3a26073002b60c91c0657ecf14120725ac3509ba3</cites><orcidid>0000-0002-0193-2526 ; 0000-0002-3886-4256 ; 0000-0002-6544-0176 ; 0000-0002-7171-6597 ; 0000-0003-2413-9392 ; 0000-0002-3377-8324 ; 0000-0001-5544-3552 ; 0000-0002-0202-0465 ; 0000-0002-8951-1127 ; 0000-0001-6769-1465 ; 0000-0003-3218-517X ; 0000-0002-5355-6657 ; 0000-0002-0499-1724 ; 0000-0001-9364-4179 ; 0000-0001-6582-1801 ; 0000-0001-6968-0110 ; 0000-0002-0125-8674 ; 0000-0002-1279-3760</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9812383/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9812383/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,2884,2885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36598988$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://hal.science/hal-04150365$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Gonen, Nitzan</creatorcontrib><creatorcontrib>Eozenou, Caroline</creatorcontrib><creatorcontrib>Mitter, Richard</creatorcontrib><creatorcontrib>Elzaiat, Maëva</creatorcontrib><creatorcontrib>Stévant, Isabelle</creatorcontrib><creatorcontrib>Aviram, Rona</creatorcontrib><creatorcontrib>Bernardo, Andreia Sofia</creatorcontrib><creatorcontrib>Chervova, Almira</creatorcontrib><creatorcontrib>Wankanit, Somboon</creatorcontrib><creatorcontrib>Frachon, Emmanuel</creatorcontrib><creatorcontrib>Commère, Pierre-Henri</creatorcontrib><creatorcontrib>Brailly-Tabard, Sylvie</creatorcontrib><creatorcontrib>Valon, Léo</creatorcontrib><creatorcontrib>Barrio Cano, Laura</creatorcontrib><creatorcontrib>Levayer, Romain</creatorcontrib><creatorcontrib>Mazen, Inas</creatorcontrib><creatorcontrib>Gobaa, Samy</creatorcontrib><creatorcontrib>Smith, James C</creatorcontrib><creatorcontrib>McElreavey, Kenneth</creatorcontrib><creatorcontrib>Lovell-Badge, Robin</creatorcontrib><creatorcontrib>Bashamboo, Anu</creatorcontrib><title>In vitro cellular reprogramming to model gonad development and its disorders</title><title>Science advances</title><addtitle>Sci Adv</addtitle><description>During embryonic development, mutually antagonistic signaling cascades determine gonadal fate toward a testicular or ovarian identity. Errors in this process result in disorders of sex development (DSDs), characterized by discordance between chromosomal, gonadal, and anatomical sex. The absence of an appropriate, accessible in vitro system is a major obstacle in understanding mechanisms of sex-determination/DSDs. Here, we describe protocols for differentiation of mouse and human pluripotent cells toward gonadal progenitors. Transcriptomic analysis reveals that the in vitro-derived murine gonadal cells are equivalent to embryonic day 11.5 in vivo progenitors. Using similar conditions, Sertoli-like cells derived from 46,XY human induced pluripotent stem cells (hiPSCs) exhibit sustained expression of testis-specific genes, secrete anti-Müllerian hormone, migrate, and form tubular structures. Cells derived from 46,XY DSD female hiPSCs, carrying an
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| fulltext | fulltext |
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| source | American Association for the Advancement of Science; PubMed Central(OpenAccess) |
| subjects | Animals Biomedicine and Life Sciences Cellular Reprogramming Cellular Reprogramming - genetics Developmental Biology Diseases and Disorders Female Gonadal Dysgenesis, 46,XY Gonadal Dysgenesis, 46,XY - genetics Gonads Humans Induced Pluripotent Stem Cells Life Sciences Male Mice SciAdv r-articles |
| title | In vitro cellular reprogramming to model gonad development and its disorders |
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