Rattus norvegicus
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ABSTRACT:
PROVIDER: PRJNA318631 | ENA |
REPOSITORIES: ENA
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Project description:The placenta is constructed through the orchestration of trophoblast stem (TS) cell expansion and differentiation along a multi-lineage pathway. Dynamic regulation of histone H3K9 methylation is pivotal to cell differentiation for many cell lineages, but little is known about its involvement in trophoblast development. Among the twelve-known histone H3K9 methyltransferases, only SUV39H2 exhibited robust differential expression in stem versus differentiated rat TS cells. SUV39H2 transcript and protein expression were high in the stem state and rapidly declined as TS cells differentiated. Disruption of SUV39H2 expression in TS cells led to prominent phenotypic changes. Suv39h2-specific shRNA knockdown resulted in an arrest in TS cell proliferation and activation of trophoblast cell differentiation. These observations were reinforced by flow cytometry and transcript profiling. Histone H3K9 methylation status at specific loci exhibiting differentiation-dependent gene expression were regulated by SUV39H2 and also represented sites for SUV39H2 occupancy. Analyses of SUV39H2 on ex vivo rat blastocyst development supported its role in regulating TS cell expansion and differentiation. Finally, we identified SUV39H2 as a downstream target of CDX2, a master regulator of trophoblast lineage development. In summary, our findings indicate that SUV39H2 contributes to the maintenance of the TS cell stem state and restrains trophoblast cell differentiation and thus serves as a contributor to the epigenetic regulation of hemochorial placental development.
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Project description:Placenta enriched 1 (PLAC1) is a highly conserved X chromosome-linked gene prominently expressed in the mammalian placenta. The functions of PLAC1 in placentation have yet to emerge fully. The rat shares hemochorial placentation and deep intrauterine trophoblast cell invasion with the human. Herein, we investigated the expression and biological activities of PLAC1 in the rat and human placenta. Plac1 transcripts were prominently expressed in the junctional zone of the rat placenta, a structure analogous to the extravillous trophoblast cell column of the human placentation site, and in invasive trophoblast cells. A PLAC1 mutant rat model was generated using CRISPR/Cas9 genome editing and used to investigate the role of PLAC1 in rat placentation. Plac1 mutant animals exhibited placentomegaly. Enlarged placentas were characterized by an expanded junctional zone, an irregular junctional zone-labyrinth zone boundary, and a prominent depletion of invasive trophoblast cells within the uterine parenchyma. PLAC1 was required for rat trophoblast stem (TS) cell differentiation. In human TS cell development, PLAC1 does not contribute to the regulation of the human invasive/extravillous trophoblast cell lineage, but instead, PLAC1 expression and actions were linked to syncytiotrophoblast differentiation. Thus, PLAC1 is critically involved in hemochorial placentation; however, the responsive trophoblast cell lineages and its contributions to placentation are fundamentally distinct in the rat versus human.
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Project description:Placenta enriched 1 (PLAC1) is a highly conserved X chromosome-linked gene prominently expressed in the mammalian placenta. The functions of PLAC1 in placentation have yet to emerge fully. The rat shares hemochorial placentation and deep intrauterine trophoblast cell invasion with the human. Herein, we investigated the expression and biological activities of PLAC1 in the rat and human placenta. Plac1 transcripts were prominently expressed in the junctional zone of the rat placenta, a structure analogous to the extravillous trophoblast cell column of the human placentation site, and in invasive trophoblast cells. A PLAC1 mutant rat model was generated using CRISPR/Cas9 genome editing and used to investigate the role of PLAC1 in rat placentation. Plac1 mutant animals exhibited placentomegaly. Enlarged placentas were characterized by an expanded junctional zone, an irregular junctional zone-labyrinth zone boundary, and a prominent depletion of invasive trophoblast cells within the uterine parenchyma. PLAC1 was required for rat trophoblast stem (TS) cell differentiation. In human TS cell development, PLAC1 does not contribute to the regulation of the human invasive/extravillous trophoblast cell lineage, but instead, PLAC1 expression and actions were linked to syncytiotrophoblast differentiation. Thus, PLAC1 is critically involved in hemochorial placentation; however, the responsive trophoblast cell lineages and its contributions to placentation are fundamentally distinct in the rat versus human.
2026-04-22 | GSE263212 | GEO
Project description:Placenta enriched 1 (PLAC1) is a highly conserved X chromosome-linked gene prominently expressed in the mammalian placenta. The functions of PLAC1 in placentation have yet to emerge fully. The rat shares hemochorial placentation and deep intrauterine trophoblast cell invasion with the human. Herein, we investigated the expression and biological activities of PLAC1 in the rat and human placenta. Plac1 transcripts were prominently expressed in the junctional zone of the rat placenta, a structure analogous to the extravillous trophoblast cell column of the human placentation site, and in invasive trophoblast cells. A PLAC1 mutant rat model was generated using CRISPR/Cas9 genome editing and used to investigate the role of PLAC1 in rat placentation. Plac1 mutant animals exhibited placentomegaly. Enlarged placentas were characterized by an expanded junctional zone, an irregular junctional zone-labyrinth zone boundary, and a prominent depletion of invasive trophoblast cells within the uterine parenchyma. PLAC1 was required for rat trophoblast stem (TS) cell differentiation. In human TS cell development, PLAC1 does not contribute to the regulation of the human invasive/extravillous trophoblast cell lineage, but instead, PLAC1 expression and actions were linked to syncytiotrophoblast differentiation. Thus, PLAC1 is critically involved in hemochorial placentation; however, the responsive trophoblast cell lineages and its contributions to placentation are fundamentally distinct in the rat versus human.
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