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this study, we have generated a null mutation in the phosphatidylserine receptor (Ptdsr) gene in C57BL/6J mice. We show that ablation of Ptdsr results in profound differentiation defects in multiple organs and tissues during embryogenesis, although with variable penetrance. While this work was in progress, two other groups reported the generation of Ptdsr-deficient mice [31,32]. In all three knockout mouse lines, the first two exons ([31] and this study) or exons one to three [32] were deleted by replacement with a neomycin-selection cassette. The Ptdsr-knockout mouse lines differ in the genetic background in which the mutation was generated and maintained, however. In our case, the Ptdsr-null allele was generated in an isogenic C57BL/6J background, whereas Li et al. [31] and Kunisaki et al. [32] investigated the phenotype of their Ptdsr-knockout mice in a mixed 129 × C57BL/6 background. The ablation of Ptdsr function results in perinatal lethality in all cases, but there are interesting differences in severity or expressivities of phenotypes among the different Ptdsr-deficient mouse lines. This might be due either to differences in genetic background or because the phenotypes that have been investigated in this study have not been analyzed in such detail before."}
craft-ca-core-ex-dev
{"project":"craft-ca-core-ex-dev","denotations":[{"id":"T9419","span":{"begin":35,"end":39},"obj":"SO_EXT:sequence_nullness"},{"id":"T9420","span":{"begin":40,"end":48},"obj":"SO_EXT:sequence_alteration_entity_or_process"},{"id":"T9421","span":{"begin":56,"end":74},"obj":"CHEBI:18303"},{"id":"T9422","span":{"begin":56,"end":83},"obj":"PR_EXT:000009218"},{"id":"T9423","span":{"begin":75,"end":83},"obj":"GO_EXT:0004872"},{"id":"T9424","span":{"begin":85,"end":90},"obj":"PR_EXT:000009218"},{"id":"T9425","span":{"begin":92,"end":96},"obj":"SO_EXT:0000704"},{"id":"T9426","span":{"begin":109,"end":113},"obj":"NCBITaxon:10088"},{"id":"T9427","span":{"begin":140,"end":145},"obj":"PR_EXT:000009218"},{"id":"T9428","span":{"begin":166,"end":181},"obj":"GO_RO_EXT:developmental_differentiation_process"},{"id":"T9429","span":{"begin":202,"end":208},"obj":"UBERON:0000062"},{"id":"T9430","span":{"begin":213,"end":220},"obj":"UBERON:0000479"},{"id":"T9431","span":{"begin":228,"end":241},"obj":"GO:0009790"},{"id":"T9432","span":{"begin":355,"end":360},"obj":"PR_EXT:000009218"},{"id":"T9433","span":{"begin":371,"end":375},"obj":"NCBITaxon:10088"},{"id":"T9434","span":{"begin":407,"end":412},"obj":"NCBITaxon:10088"},{"id":"T9435","span":{"begin":434,"end":439},"obj":"SO_EXT:0000147"},{"id":"T9436","span":{"begin":465,"end":470},"obj":"SO_EXT:0000147"},{"id":"T9437","span":{"begin":494,"end":501},"obj":"SO_EXT:sequence_deletion_process"},{"id":"T9438","span":{"begin":505,"end":516},"obj":"SO_EXT:sequence_substitution_entity_or_process"},{"id":"T9439","span":{"begin":524,"end":532},"obj":"CHEBI:7507"},{"id":"T9440","span":{"begin":543,"end":551},"obj":"SO_EXT:0005853"},{"id":"T9441","span":{"begin":557,"end":562},"obj":"PR_EXT:000009218"},{"id":"T9442","span":{"begin":572,"end":577},"obj":"NCBITaxon:10088"},{"id":"T9443","span":{"begin":598,"end":605},"obj":"SO_EXT:0000704"},{"id":"T9444","span":{"begin":630,"end":638},"obj":"SO_EXT:sequence_alteration_entity_or_process"},{"id":"T9445","span":{"begin":695,"end":700},"obj":"PR_EXT:000009218"},{"id":"T9446","span":{"begin":701,"end":705},"obj":"SO_EXT:sequence_nullness"},{"id":"T9447","span":{"begin":706,"end":712},"obj":"SO_EXT:0001023"},{"id":"T9448","span":{"begin":847,"end":852},"obj":"PR_EXT:000009218"},{"id":"T9449","span":{"begin":862,"end":866},"obj":"NCBITaxon:10088"},{"id":"T9450","span":{"begin":920,"end":925},"obj":"PR_EXT:000009218"},{"id":"T9451","span":{"begin":946,"end":955},"obj":"UBERON:0012101"},{"id":"T9452","span":{"begin":950,"end":955},"obj":"GO:0007567"},{"id":"T9453","span":{"begin":956,"end":965},"obj":"GO_EXT:fatality_or_lethality"},{"id":"T9454","span":{"begin":1082,"end":1087},"obj":"PR_EXT:000009218"},{"id":"T9455","span":{"begin":1098,"end":1103},"obj":"NCBITaxon:10088"},{"id":"T9456","span":{"begin":1154,"end":1161},"obj":"SO_EXT:0000704"}],"text":"In this study, we have generated a null mutation in the phosphatidylserine receptor (Ptdsr) gene in C57BL/6J mice. We show that ablation of Ptdsr results in profound differentiation defects in multiple organs and tissues during embryogenesis, although with variable penetrance. While this work was in progress, two other groups reported the generation of Ptdsr-deficient mice [31,32]. In all three knockout mouse lines, the first two exons ([31] and this study) or exons one to three [32] were deleted by replacement with a neomycin-selection cassette. The Ptdsr-knockout mouse lines differ in the genetic background in which the mutation was generated and maintained, however. In our case, the Ptdsr-null allele was generated in an isogenic C57BL/6J background, whereas Li et al. [31] and Kunisaki et al. [32] investigated the phenotype of their Ptdsr-knockout mice in a mixed 129 × C57BL/6 background. The ablation of Ptdsr function results in perinatal lethality in all cases, but there are interesting differences in severity or expressivities of phenotypes among the different Ptdsr-deficient mouse lines. This might be due either to differences in genetic background or because the phenotypes that have been investigated in this study have not been analyzed in such detail before."}
craft-ca-core-dev
{"project":"craft-ca-core-dev","denotations":[{"id":"T9133","span":{"begin":56,"end":74},"obj":"CHEBI:18303"},{"id":"T9134","span":{"begin":56,"end":83},"obj":"PR:000009218"},{"id":"T9135","span":{"begin":85,"end":90},"obj":"PR:000009218"},{"id":"T9136","span":{"begin":92,"end":96},"obj":"SO:0000704"},{"id":"T9137","span":{"begin":109,"end":113},"obj":"NCBITaxon:10088"},{"id":"T9138","span":{"begin":140,"end":145},"obj":"PR:000009218"},{"id":"T9139","span":{"begin":202,"end":208},"obj":"UBERON:0000062"},{"id":"T9140","span":{"begin":213,"end":220},"obj":"UBERON:0000479"},{"id":"T9141","span":{"begin":228,"end":241},"obj":"GO:0009790"},{"id":"T9142","span":{"begin":355,"end":360},"obj":"PR:000009218"},{"id":"T9143","span":{"begin":371,"end":375},"obj":"NCBITaxon:10088"},{"id":"T9144","span":{"begin":407,"end":412},"obj":"NCBITaxon:10088"},{"id":"T9145","span":{"begin":434,"end":439},"obj":"SO:0000147"},{"id":"T9146","span":{"begin":465,"end":470},"obj":"SO:0000147"},{"id":"T9147","span":{"begin":524,"end":532},"obj":"CHEBI:7507"},{"id":"T9148","span":{"begin":543,"end":551},"obj":"SO:0005853"},{"id":"T9149","span":{"begin":557,"end":562},"obj":"PR:000009218"},{"id":"T9150","span":{"begin":572,"end":577},"obj":"NCBITaxon:10088"},{"id":"T9151","span":{"begin":598,"end":605},"obj":"SO:0000704"},{"id":"T9152","span":{"begin":695,"end":700},"obj":"PR:000009218"},{"id":"T9153","span":{"begin":706,"end":712},"obj":"SO:0001023"},{"id":"T9154","span":{"begin":847,"end":852},"obj":"PR:000009218"},{"id":"T9155","span":{"begin":862,"end":866},"obj":"NCBITaxon:10088"},{"id":"T9156","span":{"begin":920,"end":925},"obj":"PR:000009218"},{"id":"T9157","span":{"begin":946,"end":955},"obj":"UBERON:0012101"},{"id":"T9158","span":{"begin":950,"end":955},"obj":"GO:0007567"},{"id":"T9159","span":{"begin":1082,"end":1087},"obj":"PR:000009218"},{"id":"T9160","span":{"begin":1098,"end":1103},"obj":"NCBITaxon:10088"},{"id":"T9161","span":{"begin":1154,"end":1161},"obj":"SO:0000704"}],"text":"In this study, we have generated a null mutation in the phosphatidylserine receptor (Ptdsr) gene in C57BL/6J mice. We show that ablation of Ptdsr results in profound differentiation defects in multiple organs and tissues during embryogenesis, although with variable penetrance. While this work was in progress, two other groups reported the generation of Ptdsr-deficient mice [31,32]. In all three knockout mouse lines, the first two exons ([31] and this study) or exons one to three [32] were deleted by replacement with a neomycin-selection cassette. The Ptdsr-knockout mouse lines differ in the genetic background in which the mutation was generated and maintained, however. In our case, the Ptdsr-null allele was generated in an isogenic C57BL/6J background, whereas Li et al. [31] and Kunisaki et al. [32] investigated the phenotype of their Ptdsr-knockout mice in a mixed 129 × C57BL/6 background. The ablation of Ptdsr function results in perinatal lethality in all cases, but there are interesting differences in severity or expressivities of phenotypes among the different Ptdsr-deficient mouse lines. This might be due either to differences in genetic background or because the phenotypes that have been investigated in this study have not been analyzed in such detail before."}
2_test
{"project":"2_test","denotations":[{"id":"15345036-14645847-55938512","span":{"begin":377,"end":379},"obj":"14645847"},{"id":"15345036-14715629-55938513","span":{"begin":380,"end":382},"obj":"14715629"},{"id":"15345036-14645847-55938514","span":{"begin":442,"end":444},"obj":"14645847"},{"id":"15345036-14715629-55938515","span":{"begin":485,"end":487},"obj":"14715629"},{"id":"15345036-14645847-55938516","span":{"begin":782,"end":784},"obj":"14645847"},{"id":"15345036-14715629-55938517","span":{"begin":807,"end":809},"obj":"14715629"}],"text":"In this study, we have generated a null mutation in the phosphatidylserine receptor (Ptdsr) gene in C57BL/6J mice. We show that ablation of Ptdsr results in profound differentiation defects in multiple organs and tissues during embryogenesis, although with variable penetrance. While this work was in progress, two other groups reported the generation of Ptdsr-deficient mice [31,32]. In all three knockout mouse lines, the first two exons ([31] and this study) or exons one to three [32] were deleted by replacement with a neomycin-selection cassette. The Ptdsr-knockout mouse lines differ in the genetic background in which the mutation was generated and maintained, however. In our case, the Ptdsr-null allele was generated in an isogenic C57BL/6J background, whereas Li et al. [31] and Kunisaki et al. [32] investigated the phenotype of their Ptdsr-knockout mice in a mixed 129 × C57BL/6 background. The ablation of Ptdsr function results in perinatal lethality in all cases, but there are interesting differences in severity or expressivities of phenotypes among the different Ptdsr-deficient mouse lines. This might be due either to differences in genetic background or because the phenotypes that have been investigated in this study have not been analyzed in such detail before."}