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joins an expanding list of mouse genes for which targeted disruption results in peri-implantation lethality as a result of trophoblast or placental abnormalities (reviewed in [25]). Comparison with other phenotypes might provide some insight into the role of Atrx in trophoblast development. Atrx-mutant embryos progress further than embryos nullizygous for factors involved in the initial specification of trophoblast stem cells (such as Cdx2) or in stem cell maintenance and proliferation (such as Eomes). Cdx2-mutant embryos fail to implant and die between 3.5 and 5.5 dpc [26], while Eomes-mutant blastocysts implant into the uterus, but arrest soon after implantation without forming organised embryonic or extraembryonic structures [27]. In contrast, Atrx-mutant embryos implant successfully and establish organised embryonic structures by 7.5 dpc. The Atrx-mutant phenotype closely resembles that observed in mice nullizygous for the basic helix-loop-helix transcription factor Hand1. Hand1-mutant conceptuses arrest at around 7.5 dpc and display a normal embryonic compartment, but, like Atrx-mutant embryos, ablation of Hand1 causes a reduction in the size of the ectoplacental cone and density of TGCs [28]. As with Atrx mutants, only arrested or resorbed Hand1-mutant conceptuses were recovered after 8.5 dpc. Also like Atrx, disruption of Hand1 specifically affects secondary giant cell formation, and primary trophoblast outgrowths from blastocysts appeared normal. Hand1 is required for terminal differentiation of secondary TGCs, and in its absence trophoblast cells arrest at a precursor stage in the ectoplacental cone [17,28]. Given the similarity of the Atrx- and Hand1-mutant phenotypes and the likelihood that Atrx acts as a transcriptional regulator by modifying chromatin structure, it will be of interest to determine whether Atrx is itself a regulator of Hand1 expression, or alternatively whether it acts as a co-regulator of one or more of the downstream transcriptional targets of Hand1. It is noteworthy that, in the brain-specific Atrx knockout mice, the defect was observed in terminally differentiating neurons [20]. The secondary TGCs affected in the universal Atrx knockout reported here represent one of the first terminally differentiated tissues in the developing mouse, and this may point to the requirement for Atrx in the high-level expression of some tissue-specific genes during the final stages of differentiation. Interestingly, the α-globin genes, the only confirmed transcriptional targets of regulation by human ATRX, are also highly expressed specifically during terminal differentiation within the erythroid lineage.\n"}

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joins an expanding list of mouse genes for which targeted disruption results in peri-implantation lethality as a result of trophoblast or placental abnormalities (reviewed in [25]). Comparison with other phenotypes might provide some insight into the role of Atrx in trophoblast development. Atrx-mutant embryos progress further than embryos nullizygous for factors involved in the initial specification of trophoblast stem cells (such as Cdx2) or in stem cell maintenance and proliferation (such as Eomes). Cdx2-mutant embryos fail to implant and die between 3.5 and 5.5 dpc [26], while Eomes-mutant blastocysts implant into the uterus, but arrest soon after implantation without forming organised embryonic or extraembryonic structures [27]. In contrast, Atrx-mutant embryos implant successfully and establish organised embryonic structures by 7.5 dpc. The Atrx-mutant phenotype closely resembles that observed in mice nullizygous for the basic helix-loop-helix transcription factor Hand1. Hand1-mutant conceptuses arrest at around 7.5 dpc and display a normal embryonic compartment, but, like Atrx-mutant embryos, ablation of Hand1 causes a reduction in the size of the ectoplacental cone and density of TGCs [28]. As with Atrx mutants, only arrested or resorbed Hand1-mutant conceptuses were recovered after 8.5 dpc. Also like Atrx, disruption of Hand1 specifically affects secondary giant cell formation, and primary trophoblast outgrowths from blastocysts appeared normal. Hand1 is required for terminal differentiation of secondary TGCs, and in its absence trophoblast cells arrest at a precursor stage in the ectoplacental cone [17,28]. Given the similarity of the Atrx- and Hand1-mutant phenotypes and the likelihood that Atrx acts as a transcriptional regulator by modifying chromatin structure, it will be of interest to determine whether Atrx is itself a regulator of Hand1 expression, or alternatively whether it acts as a co-regulator of one or more of the downstream transcriptional targets of Hand1. It is noteworthy that, in the brain-specific Atrx knockout mice, the defect was observed in terminally differentiating neurons [20]. The secondary TGCs affected in the universal Atrx knockout reported here represent one of the first terminally differentiated tissues in the developing mouse, and this may point to the requirement for Atrx in the high-level expression of some tissue-specific genes during the final stages of differentiation. Interestingly, the α-globin genes, the only confirmed transcriptional targets of regulation by human ATRX, are also highly expressed specifically during terminal differentiation within the erythroid lineage.\n"}

{"project":"2_test","denotations":[{"id":"16628246-11433360-85799766","span":{"begin":181,"end":183},"obj":"11433360"},{"id":"16628246-9052785-85799767","span":{"begin":582,"end":584},"obj":"9052785"},{"id":"16628246-10716450-85799768","span":{"begin":744,"end":746},"obj":"10716450"},{"id":"16628246-9500551-85799769","span":{"begin":1218,"end":1220},"obj":"9500551"},{"id":"16628246-10611232-85799770","span":{"begin":1642,"end":1644},"obj":"10611232"},{"id":"16628246-9500551-85799771","span":{"begin":1645,"end":1647},"obj":"9500551"},{"id":"16628246-15668733-85799772","span":{"begin":2149,"end":2151},"obj":"15668733"},{"id":"T36669","span":{"begin":181,"end":183},"obj":"11433360"},{"id":"T78131","span":{"begin":582,"end":584},"obj":"9052785"},{"id":"T46656","span":{"begin":744,"end":746},"obj":"10716450"},{"id":"T27799","span":{"begin":1218,"end":1220},"obj":"9500551"},{"id":"T13124","span":{"begin":1642,"end":1644},"obj":"10611232"},{"id":"T42247","span":{"begin":1645,"end":1647},"obj":"9500551"},{"id":"T83367","span":{"begin":2149,"end":2151},"obj":"15668733"}],"text":"Atrx joins an expanding list of mouse genes for which targeted disruption results in peri-implantation lethality as a result of trophoblast or placental abnormalities (reviewed in [25]). Comparison with other phenotypes might provide some insight into the role of Atrx in trophoblast development. Atrx-mutant embryos progress further than embryos nullizygous for factors involved in the initial specification of trophoblast stem cells (such as Cdx2) or in stem cell maintenance and proliferation (such as Eomes). Cdx2-mutant embryos fail to implant and die between 3.5 and 5.5 dpc [26], while Eomes-mutant blastocysts implant into the uterus, but arrest soon after implantation without forming organised embryonic or extraembryonic structures [27]. In contrast, Atrx-mutant embryos implant successfully and establish organised embryonic structures by 7.5 dpc. The Atrx-mutant phenotype closely resembles that observed in mice nullizygous for the basic helix-loop-helix transcription factor Hand1. Hand1-mutant conceptuses arrest at around 7.5 dpc and display a normal embryonic compartment, but, like Atrx-mutant embryos, ablation of Hand1 causes a reduction in the size of the ectoplacental cone and density of TGCs [28]. As with Atrx mutants, only arrested or resorbed Hand1-mutant conceptuses were recovered after 8.5 dpc. Also like Atrx, disruption of Hand1 specifically affects secondary giant cell formation, and primary trophoblast outgrowths from blastocysts appeared normal. Hand1 is required for terminal differentiation of secondary TGCs, and in its absence trophoblast cells arrest at a precursor stage in the ectoplacental cone [17,28]. Given the similarity of the Atrx- and Hand1-mutant phenotypes and the likelihood that Atrx acts as a transcriptional regulator by modifying chromatin structure, it will be of interest to determine whether Atrx is itself a regulator of Hand1 expression, or alternatively whether it acts as a co-regulator of one or more of the downstream transcriptional targets of Hand1. It is noteworthy that, in the brain-specific Atrx knockout mice, the defect was observed in terminally differentiating neurons [20]. The secondary TGCs affected in the universal Atrx knockout reported here represent one of the first terminally differentiated tissues in the developing mouse, and this may point to the requirement for Atrx in the high-level expression of some tissue-specific genes during the final stages of differentiation. Interestingly, the α-globin genes, the only confirmed transcriptional targets of regulation by human ATRX, are also highly expressed specifically during terminal differentiation within the erythroid lineage.\n"}

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joins an expanding list of mouse genes for which targeted disruption results in peri-implantation lethality as a result of trophoblast or placental abnormalities (reviewed in [25]). Comparison with other phenotypes might provide some insight into the role of Atrx in trophoblast development. Atrx-mutant embryos progress further than embryos nullizygous for factors involved in the initial specification of trophoblast stem cells (such as Cdx2) or in stem cell maintenance and proliferation (such as Eomes). Cdx2-mutant embryos fail to implant and die between 3.5 and 5.5 dpc [26], while Eomes-mutant blastocysts implant into the uterus, but arrest soon after implantation without forming organised embryonic or extraembryonic structures [27]. In contrast, Atrx-mutant embryos implant successfully and establish organised embryonic structures by 7.5 dpc. The Atrx-mutant phenotype closely resembles that observed in mice nullizygous for the basic helix-loop-helix transcription factor Hand1. Hand1-mutant conceptuses arrest at around 7.5 dpc and display a normal embryonic compartment, but, like Atrx-mutant embryos, ablation of Hand1 causes a reduction in the size of the ectoplacental cone and density of TGCs [28]. As with Atrx mutants, only arrested or resorbed Hand1-mutant conceptuses were recovered after 8.5 dpc. Also like Atrx, disruption of Hand1 specifically affects secondary giant cell formation, and primary trophoblast outgrowths from blastocysts appeared normal. Hand1 is required for terminal differentiation of secondary TGCs, and in its absence trophoblast cells arrest at a precursor stage in the ectoplacental cone [17,28]. Given the similarity of the Atrx- and Hand1-mutant phenotypes and the likelihood that Atrx acts as a transcriptional regulator by modifying chromatin structure, it will be of interest to determine whether Atrx is itself a regulator of Hand1 expression, or alternatively whether it acts as a co-regulator of one or more of the downstream transcriptional targets of Hand1. It is noteworthy that, in the brain-specific Atrx knockout mice, the defect was observed in terminally differentiating neurons [20]. The secondary TGCs affected in the universal Atrx knockout reported here represent one of the first terminally differentiated tissues in the developing mouse, and this may point to the requirement for Atrx in the high-level expression of some tissue-specific genes during the final stages of differentiation. Interestingly, the α-globin genes, the only confirmed transcriptional targets of regulation by human ATRX, are also highly expressed specifically during terminal differentiation within the erythroid lineage.\n"}