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has been known for many years that Rb loss perturbs neuronal differentiation [26–29]. However, prior work could not exclude the possibility that differentiation defects are simply an indirect consequence of abnormal division and death. If Rb does regulate differentiation directly it is unclear whether it does so in all or a subset of neurons. Moreover, the mechanism has never been solved. In other cell types where Rb may promote differentiation directly, such as muscle and bone, it seems to do so through E2f-independent means by potentiating tissue-specific transcription factors (Figure 1B) [30–33]. In the retina, others have noted abnormally shaped Rb KO rods and have suggested Rb may directly promote their morphogenesis by activating retina-specific factors [29]. However, differentiation defects in any Rb KO neuron could be an indirect effect of ectopic division and/or apoptosis (Figure 1B). Thus, it is critical to study differentiation of Rb KO cells in the absence of ectopic proliferation and death."}

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{"project":"2_test","denotations":[{"id":"17608565-1406933-84868962","span":{"begin":81,"end":83},"obj":"1406933"},{"id":"17608565-1406932-84868962","span":{"begin":81,"end":83},"obj":"1406932"},{"id":"17608565-7958874-84868962","span":{"begin":81,"end":83},"obj":"7958874"},{"id":"17608565-14991054-84868962","span":{"begin":81,"end":83},"obj":"14991054"},{"id":"17608565-9420334-84868963","span":{"begin":602,"end":604},"obj":"9420334"},{"id":"17608565-8381715-84868963","span":{"begin":602,"end":604},"obj":"8381715"},{"id":"17608565-11545733-84868963","span":{"begin":602,"end":604},"obj":"11545733"},{"id":"17608565-8946919-84868963","span":{"begin":602,"end":604},"obj":"8946919"},{"id":"17608565-14991054-84868964","span":{"begin":774,"end":776},"obj":"14991054"},{"id":"T28488","span":{"begin":81,"end":83},"obj":"1406933"},{"id":"T94522","span":{"begin":81,"end":83},"obj":"1406932"},{"id":"T38375","span":{"begin":81,"end":83},"obj":"7958874"},{"id":"T411","span":{"begin":81,"end":83},"obj":"14991054"},{"id":"T42910","span":{"begin":602,"end":604},"obj":"9420334"},{"id":"T60785","span":{"begin":602,"end":604},"obj":"8381715"},{"id":"T17937","span":{"begin":602,"end":604},"obj":"11545733"},{"id":"T32658","span":{"begin":602,"end":604},"obj":"8946919"},{"id":"T89272","span":{"begin":774,"end":776},"obj":"14991054"}],"text":"It has been known for many years that Rb loss perturbs neuronal differentiation [26–29]. However, prior work could not exclude the possibility that differentiation defects are simply an indirect consequence of abnormal division and death. If Rb does regulate differentiation directly it is unclear whether it does so in all or a subset of neurons. Moreover, the mechanism has never been solved. In other cell types where Rb may promote differentiation directly, such as muscle and bone, it seems to do so through E2f-independent means by potentiating tissue-specific transcription factors (Figure 1B) [30–33]. In the retina, others have noted abnormally shaped Rb KO rods and have suggested Rb may directly promote their morphogenesis by activating retina-specific factors [29]. However, differentiation defects in any Rb KO neuron could be an indirect effect of ectopic division and/or apoptosis (Figure 1B). Thus, it is critical to study differentiation of Rb KO cells in the absence of ectopic proliferation and death."}