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Regulates SAC Differentiation through E2f3a\nTo test which E2f3 isoform is responsible for aberrant Rb KO SAC differentiation we exploited E2f3a−/− mice (Figure 7A). The genotyping strategy outlined in Figure 7A was used to distinguish the E2f3a, WT, and null alleles. Reverse transcriptase PCR (RT-PCR) confirmed the presence of both E2f3a and E2f3b RNA species in the developing WT retina, and the specific absence of E2f3a RNA in the E2f3a−/− retina (Figure 7B). E2f3a protein was absent in E2f3a−/− retinal lysate (Figures 6 and S8). Importantly, the levels of E2f3b message were similar in the Rb KO and Rb/E2f3a DKO retina, ruling out the possibility that any effects of E2f3a deletion we might observe were due to down-regulation of E2f3b (Figure 7C). Also, the levels of other E2fs were the same in the Rb KO, Rb/E2f3 DKO, and Rb/E2f3a DKO retina, ruling out any cross-regulatory effects (Figure 7C) [55]. E2f3a can trigger cell cycle induction, but because SAC defects are not linked to cell cycle perturbation (Figures 3A and 4), and in view of the predominant association between E2f3b and Rb in quiescent cells [16,19], we suspected that E2f3b may perturb differentiation in Rb KO SACs. Unexpectedly, however, E2f3a deletion suppressed the Rb KO SAC defect (Figure 7D). Thus, separate from its role in cell cycle control, Rb regulation of E2f3a is critical to ensure proper neuronal differentiation."}

{"project":"craft-ca-core-ex-dev","denotations":[{"id":"T21433","span":{"begin":271,"end":292},"obj":"GO_EXT:0003964"},{"id":"T21417","span":{"begin":0,"end":2},"obj":"PR_EXT:000013773"},{"id":"T21419","span":{"begin":17,"end":32},"obj":"GO_RO_EXT:developmental_differentiation_process"},{"id":"T21420","span":{"begin":41,"end":46},"obj":"PR_EXT:000028775"},{"id":"T21421","span":{"begin":61,"end":65},"obj":"PR_EXT:000006854"},{"id":"T21422","span":{"begin":66,"end":73},"obj":"SO_EXT:0001060"},{"id":"T21423","span":{"begin":102,"end":104},"obj":"PR_EXT:000013773"},{"id":"T21424","span":{"begin":112,"end":127},"obj":"GO_RO_EXT:developmental_differentiation_process"},{"id":"T21425","span":{"begin":141,"end":146},"obj":"PR_EXT:000028775"},{"id":"T21426","span":{"begin":146,"end":147},"obj":"SO_EXT:sequence_nullness_or_absence"},{"id":"T21427","span":{"begin":148,"end":149},"obj":"SO_EXT:sequence_nullness_or_absence"},{"id":"T21428","span":{"begin":150,"end":154},"obj":"NCBITaxon:10088"},{"id":"T21429","span":{"begin":242,"end":247},"obj":"PR_EXT:000028775"},{"id":"T21430","span":{"begin":249,"end":251},"obj":"SO_EXT:wild_type_entity_or_quality"},{"id":"T21431","span":{"begin":257,"end":261},"obj":"SO_EXT:sequence_nullness"},{"id":"T21432","span":{"begin":262,"end":269},"obj":"SO_EXT:0001023"},{"id":"T21434","span":{"begin":298,"end":300},"obj":"GO_EXT:reverse_transcription_or_reverse_transcriptase"},{"id":"T21435","span":{"begin":337,"end":342},"obj":"PR_EXT:000028775"},{"id":"T21436","span":{"begin":353,"end":356},"obj":"CHEBI_SO_EXT:RNA"},{"id":"T21437","span":{"begin":383,"end":385},"obj":"SO_EXT:wild_type_entity_or_quality"},{"id":"T21438","span":{"begin":386,"end":392},"obj":"UBERON:0000966"},{"id":"T21439","span":{"begin":422,"end":427},"obj":"PR_EXT:000028775"},{"id":"T21440","span":{"begin":428,"end":431},"obj":"CHEBI_SO_EXT:RNA"},{"id":"T21441","span":{"begin":439,"end":444},"obj":"PR_EXT:000028775"},{"id":"T21442","span":{"begin":444,"end":445},"obj":"SO_EXT:sequence_nullness_or_absence"},{"id":"T21443","span":{"begin":446,"end":447},"obj":"SO_EXT:sequence_nullness_or_absence"},{"id":"T21444","span":{"begin":448,"end":454},"obj":"UBERON:0000966"},{"id":"T21445","span":{"begin":468,"end":473},"obj":"PR_EXT:000028775"},{"id":"T21446","span":{"begin":474,"end":481},"obj":"CHEBI_PR_EXT:protein"},{"id":"T21447","span":{"begin":496,"end":501},"obj":"PR_EXT:000028775"},{"id":"T21448","span":{"begin":501,"end":502},"obj":"SO_EXT:sequence_nullness_or_absence"},{"id":"T21449","span":{"begin":503,"end":504},"obj":"SO_EXT:sequence_nullness_or_absence"},{"id":"T21450","span":{"begin":505,"end":512},"obj":"UBERON:0000966"},{"id":"T21451","span":{"begin":573,"end":580},"obj":"SO_EXT:0000673"},{"id":"T21452","span":{"begin":573,"end":580},"obj":"CHEBI:33695"},{"id":"T21453","span":{"begin":601,"end":603},"obj":"PR_EXT:000013773"},{"id":"T21454","span":{"begin":611,"end":613},"obj":"PR_EXT:000013773"},{"id":"T21455","span":{"begin":614,"end":619},"obj":"PR_EXT:000028775"},{"id":"T21456","span":{"begin":624,"end":630},"obj":"UBERON:0000966"},{"id":"T21457","span":{"begin":679,"end":684},"obj":"PR_EXT:000028775"},{"id":"T21458","span":{"begin":685,"end":693},"obj":"SO_EXT:sequence_deletion_entity_or_process"},{"id":"T21459","span":{"begin":723,"end":738},"obj":"GO_EXT:negative_regulation"},{"id":"T21460","span":{"begin":787,"end":791},"obj":"PR_EXT:E2F"},{"id":"T21461","span":{"begin":813,"end":815},"obj":"PR_EXT:000013773"},{"id":"T21462","span":{"begin":820,"end":822},"obj":"PR_EXT:000013773"},{"id":"T21463","span":{"begin":823,"end":827},"obj":"PR_EXT:000006854"},{"id":"T21464","span":{"begin":837,"end":839},"obj":"PR_EXT:000013773"},{"id":"T21465","span":{"begin":840,"end":845},"obj":"PR_EXT:000028775"},{"id":"T21466","span":{"begin":850,"end":856},"obj":"UBERON:0000966"},{"id":"T21467","span":{"begin":879,"end":889},"obj":"GO:0065007"},{"id":"T21468","span":{"begin":916,"end":921},"obj":"PR_EXT:000028775"},{"id":"T21469","span":{"begin":934,"end":938},"obj":"CL_GO_EXT:cell"},{"id":"T21470","span":{"begin":934,"end":944},"obj":"GO:0007049"},{"id":"T21471","span":{"begin":998,"end":1002},"obj":"CL_GO_EXT:cell"},{"id":"T21472","span":{"begin":998,"end":1008},"obj":"GO:0007049"},{"id":"T21473","span":{"begin":1103,"end":1105},"obj":"PR_EXT:000013773"},{"id":"T21474","span":{"begin":1109,"end":1118},"obj":"GO:0044838"},{"id":"T21475","span":{"begin":1119,"end":1124},"obj":"CL_GO_EXT:cell"},{"id":"T21476","span":{"begin":1170,"end":1185},"obj":"GO_RO_EXT:developmental_differentiation_process"},{"id":"T21477","span":{"begin":1189,"end":1191},"obj":"PR_EXT:000013773"},{"id":"T21478","span":{"begin":1224,"end":1229},"obj":"PR_EXT:000028775"},{"id":"T21479","span":{"begin":1230,"end":1238},"obj":"SO_EXT:sequence_deletion_entity_or_process"},{"id":"T21480","span":{"begin":1254,"end":1256},"obj":"PR_EXT:000013773"},{"id":"T21481","span":{"begin":1316,"end":1320},"obj":"CL_GO_EXT:cell"},{"id":"T21482","span":{"begin":1316,"end":1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Regulates SAC Differentiation through E2f3a\nTo test which E2f3 isoform is responsible for aberrant Rb KO SAC differentiation we exploited E2f3a−/− mice (Figure 7A). The genotyping strategy outlined in Figure 7A was used to distinguish the E2f3a, WT, and null alleles. Reverse transcriptase PCR (RT-PCR) confirmed the presence of both E2f3a and E2f3b RNA species in the developing WT retina, and the specific absence of E2f3a RNA in the E2f3a−/− retina (Figure 7B). E2f3a protein was absent in E2f3a−/− retinal lysate (Figures 6 and S8). Importantly, the levels of E2f3b message were similar in the Rb KO and Rb/E2f3a DKO retina, ruling out the possibility that any effects of E2f3a deletion we might observe were due to down-regulation of E2f3b (Figure 7C). Also, the levels of other E2fs were the same in the Rb KO, Rb/E2f3 DKO, and Rb/E2f3a DKO retina, ruling out any cross-regulatory effects (Figure 7C) [55]. E2f3a can trigger cell cycle induction, but because SAC defects are not linked to cell cycle perturbation (Figures 3A and 4), and in view of the predominant association between E2f3b and Rb in quiescent cells [16,19], we suspected that E2f3b may perturb differentiation in Rb KO SACs. Unexpectedly, however, E2f3a deletion suppressed the Rb KO SAC defect (Figure 7D). Thus, separate from its role in cell cycle control, Rb regulation of E2f3a is critical to ensure proper neuronal differentiation."}

{"project":"craft-ca-core-dev","denotations":[{"id":"T21372","span":{"begin":0,"end":2},"obj":"PR:000013773"},{"id":"T21373","span":{"begin":3,"end":12},"obj":"GO:0065007"},{"id":"T21374","span":{"begin":41,"end":46},"obj":"PR:000028775"},{"id":"T21375","span":{"begin":61,"end":65},"obj":"PR:000006854"},{"id":"T21376","span":{"begin":66,"end":73},"obj":"SO:0001060"},{"id":"T21377","span":{"begin":102,"end":104},"obj":"PR:000013773"},{"id":"T21378","span":{"begin":141,"end":146},"obj":"PR:000028775"},{"id":"T21379","span":{"begin":150,"end":154},"obj":"NCBITaxon:10088"},{"id":"T21380","span":{"begin":242,"end":247},"obj":"PR:000028775"},{"id":"T21381","span":{"begin":262,"end":269},"obj":"SO:0001023"},{"id":"T21382","span":{"begin":337,"end":342},"obj":"PR:000028775"},{"id":"T21383","span":{"begin":386,"end":392},"obj":"UBERON:0000966"},{"id":"T21384","span":{"begin":422,"end":427},"obj":"PR:000028775"},{"id":"T21385","span":{"begin":439,"end":444},"obj":"PR:000028775"},{"id":"T21386","span":{"begin":448,"end":454},"obj":"UBERON:0000966"},{"id":"T21387","span":{"begin":468,"end":473},"obj":"PR:000028775"},{"id":"T21388","span":{"begin":496,"end":501},"obj":"PR:000028775"},{"id":"T21389","span":{"begin":505,"end":512},"obj":"UBERON:0000966"},{"id":"T21390","span":{"begin":573,"end":580},"obj":"SO:0000673"},{"id":"T21391","span":{"begin":573,"end":580},"obj":"CHEBI:33695"},{"id":"T21392","span":{"begin":601,"end":603},"obj":"PR:000013773"},{"id":"T21393","span":{"begin":611,"end":613},"obj":"PR:000013773"},{"id":"T21394","span":{"begin":614,"end":619},"obj":"PR:000028775"},{"id":"T21395","span":{"begin":624,"end":630},"obj":"UBERON:0000966"},{"id":"T21396","span":{"begin":679,"end":684},"obj":"PR:000028775"},{"id":"T21397","span":{"begin":813,"end":815},"obj":"PR:000013773"},{"id":"T21398","span":{"begin":820,"end":822},"obj":"PR:000013773"},{"id":"T21399","span":{"begin":823,"end":827},"obj":"PR:000006854"},{"id":"T21400","span":{"begin":837,"end":839},"obj":"PR:000013773"},{"id":"T21401","span":{"begin":840,"end":845},"obj":"PR:000028775"},{"id":"T21402","span":{"begin":850,"end":856},"obj":"UBERON:0000966"},{"id":"T21403","span":{"begin":879,"end":889},"obj":"GO:0065007"},{"id":"T21404","span":{"begin":916,"end":921},"obj":"PR:000028775"},{"id":"T21405","span":{"begin":934,"end":944},"obj":"GO:0007049"},{"id":"T21406","span":{"begin":998,"end":1008},"obj":"GO:0007049"},{"id":"T21407","span":{"begin":1103,"end":1105},"obj":"PR:000013773"},{"id":"T21408","span":{"begin":1109,"end":1118},"obj":"GO:0044838"},{"id":"T21409","span":{"begin":1189,"end":1191},"obj":"PR:000013773"},{"id":"T21410","span":{"begin":1224,"end":1229},"obj":"PR:000028775"},{"id":"T21411","span":{"begin":1254,"end":1256},"obj":"PR:000013773"},{"id":"T21412","span":{"begin":1316,"end":1334},"obj":"GO:0051726"},{"id":"T21413","span":{"begin":1336,"end":1338},"obj":"PR:000013773"},{"id":"T21414","span":{"begin":1339,"end":1349},"obj":"GO:0065007"},{"id":"T21415","span":{"begin":1353,"end":1358},"obj":"PR:000028775"},{"id":"T21416","span":{"begin":1388,"end":1396},"obj":"CL:0000540"}],"text":"Rb Regulates SAC Differentiation through E2f3a\nTo test which E2f3 isoform is responsible for aberrant Rb KO SAC differentiation we exploited E2f3a−/− mice (Figure 7A). The genotyping strategy outlined in Figure 7A was used to distinguish the E2f3a, WT, and null alleles. Reverse transcriptase PCR (RT-PCR) confirmed the presence of both E2f3a and E2f3b RNA species in the developing WT retina, and the specific absence of E2f3a RNA in the E2f3a−/− retina (Figure 7B). E2f3a protein was absent in E2f3a−/− retinal lysate (Figures 6 and S8). Importantly, the levels of E2f3b message were similar in the Rb KO and Rb/E2f3a DKO retina, ruling out the possibility that any effects of E2f3a deletion we might observe were due to down-regulation of E2f3b (Figure 7C). Also, the levels of other E2fs were the same in the Rb KO, Rb/E2f3 DKO, and Rb/E2f3a DKO retina, ruling out any cross-regulatory effects (Figure 7C) [55]. E2f3a can trigger cell cycle induction, but because SAC defects are not linked to cell cycle perturbation (Figures 3A and 4), and in view of the predominant association between E2f3b and Rb in quiescent cells [16,19], we suspected that E2f3b may perturb differentiation in Rb KO SACs. Unexpectedly, however, E2f3a deletion suppressed the Rb KO SAC defect (Figure 7D). Thus, separate from its role in cell cycle control, Rb regulation of E2f3a is critical to ensure proper neuronal differentiation."}

{"project":"2_test","denotations":[{"id":"17608565-16909124-84869005","span":{"begin":911,"end":913},"obj":"16909124"},{"id":"17608565-10779352-84869006","span":{"begin":1126,"end":1128},"obj":"10779352"},{"id":"17608565-15175242-84869007","span":{"begin":1129,"end":1131},"obj":"15175242"},{"id":"T75502","span":{"begin":911,"end":913},"obj":"16909124"},{"id":"T75730","span":{"begin":1126,"end":1128},"obj":"10779352"},{"id":"T58568","span":{"begin":1129,"end":1131},"obj":"15175242"}],"text":"Rb Regulates SAC Differentiation through E2f3a\nTo test which E2f3 isoform is responsible for aberrant Rb KO SAC differentiation we exploited E2f3a−/− mice (Figure 7A). The genotyping strategy outlined in Figure 7A was used to distinguish the E2f3a, WT, and null alleles. Reverse transcriptase PCR (RT-PCR) confirmed the presence of both E2f3a and E2f3b RNA species in the developing WT retina, and the specific absence of E2f3a RNA in the E2f3a−/− retina (Figure 7B). E2f3a protein was absent in E2f3a−/− retinal lysate (Figures 6 and S8). Importantly, the levels of E2f3b message were similar in the Rb KO and Rb/E2f3a DKO retina, ruling out the possibility that any effects of E2f3a deletion we might observe were due to down-regulation of E2f3b (Figure 7C). Also, the levels of other E2fs were the same in the Rb KO, Rb/E2f3 DKO, and Rb/E2f3a DKO retina, ruling out any cross-regulatory effects (Figure 7C) [55]. E2f3a can trigger cell cycle induction, but because SAC defects are not linked to cell cycle perturbation (Figures 3A and 4), and in view of the predominant association between E2f3b and Rb in quiescent cells [16,19], we suspected that E2f3b may perturb differentiation in Rb KO SACs. Unexpectedly, however, E2f3a deletion suppressed the Rb KO SAC defect (Figure 7D). Thus, separate from its role in cell cycle control, Rb regulation of E2f3a is critical to ensure proper neuronal differentiation."}