Abstract
During central nervous system (CNS) development, genetic programs establish neural stem cells and drive both stem and daughter cell proliferation. However, the prominent anterior expansion of the CNS implies anterior–posterior (A–P) modulation of these programs. In Drosophila, a set of neural stem cell factors acts along the entire A–P axis to establish neural stem cells. Brain expansion results from enhanced stem and daughter cell proliferation, promoted by a Polycomb Group (PcG)->Homeobox (Hox) homeotic network. But how does PcG->Hox modulate neural-stem-cell–factor activity along the A–P axis? We find that the PcG->Hox network creates an A–P expression gradient of neural stem cell factors, thereby driving a gradient of proliferation. PcG mutants can be rescued by misexpression of the neural stem cell factors or by mutation of one single Hox gene. Hence, brain expansion results from anterior enhancement of core neural-stem-cell–factor expression, mediated by PcG repression of brain Hox expression.
Highlights
During central nervous system (CNS) development, neural progenitor cells undergo repetitive rounds of asymmetric cell divisions, renewing themselves and generating daughter cells
Hox genes act in an antiproliferative manner, which explains the hyperproliferation observed in the brain, as well as the gradient of proliferation along the anterior–posterior axis of the central nervous system
We find that Hox genes act by repressing a common neural stem cell proliferation program in more posterior regions, resulting in an anterior–posterior gradient of “stemness.” elevated anterior proliferation is promoted by the Polycomb Group Complex acting to keep the brain free of negative Hox input, thereby
Summary
During central nervous system (CNS) development, neural progenitor cells undergo repetitive rounds of asymmetric cell divisions, renewing themselves and generating daughter cells. Studies have revealed profound differences in both progenitor and daughter cell proliferation behavior when comparing along the anterior–posterior (A–P) axis and over developmental time [1,2,3,4,5,6,7] Such differences can result in striking alterations in lineage size when comparing between different progenitors, from a few to several hundred cells generated from one progenitor [8,9,10,11,12,13]. How neural progenitor and daughter cell proliferation is modified along the A–P axis and over developmental time to thereby result in changes in lineage and regional CNS size is still poorly understood
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