Summary

1. Cells release hedgehog (hh) to trigger and propagate the morphogenetic furrow across the developing fruit fly eye. Within each ommatidium, one cell outcompetes others to become photoreceptor 8 (R8), which then directs differentiation of the other photoreceptors, culminating in the expression of bride of sevenless (boss) to activate sevenless, a receptor tyrosine kinase (RTK) in photoreceptor R7. See Figures 4.2–4.4
2. In the developing vertebrate neural tube, cell-cell interactions include the release of BMP that pushes cells to become glia, the release of FGFs that push cells to become neurons, and Delta-Notch signaling between cells in contact with one another. These result in a mix of neurons and glia. See Figures 4.5 and 4.6
Spinal motor neurons are first induced by exposure to moderate levels of Sonic hedgehog (Shh) from the notochord and floor plate. All the cells that will become motor neurons express homeotic genes Isl-1 and Isl-2
3. during early differentiation, then express different combinations of transcription factors to differentiate into different subpopulations innervating various targets. They also express different Hox genes at anterior-posterior levels. See Figures 4.7–4.9
4. Neural crest cells migrate to many different parts of the body to take on different roles. Their differentiation is guided by exposure to factors from other cells along their routes, at their destinations, and from their innervation targets. Crest cells transplanted from one segment of the anterior-posterior axis to another take on the fate appropriate to their new position. See Figure 4.10
5. If crest cells encounter axons in the periphery, that contact induces them to differentiate into Schwann cells providing myelin. In Hansen’s disease, infected Schwann cells dedifferentiate to revert to migratory behavior, thereby spreading infection to the skin, which forms granulomas in response. See Figure 4.11
6. The subset of sympathetic postganglionic neurons that innervate sweat glands are directed by their target to switch from using norepinephrine (NE) to using acetylcholine (ACh) as a neurotransmitter. See Figure 4.12
7. In mammalian neocortex, cells migrate from the ventricular zone to none of six layers, differentiating into the appropriate neuronal phenotypes. Transplant studies show that shortly after becoming postmitotic, a cell is instructed by the ventricular zone to migrate to a particular layer; prior to that time, it can migrate to the end of the radial glia and then take on the fate appropriate to whatever layer is forming there. See Figure 4.13
8. The many transcription factors that direct neural differentiation often interact, affecting each other’s transcription and/or protein activity, which is probably responsible for the extremely wide diversity of structure and function in neurons and glia. See Figure 4.14
9. Larger brains tend to evolve as a result of prolonged later embryonic stages that result in more cells and/or more elaborate neural processes found in later-arising structures, such as the outer layers of neocortex in mammals and the prefrontal cortex in primates. See Figures 4.15 and 4.16
10. The evolution of humans from an ancestor in common with the other apes may have been driven by neoteny, extending fetal-typical brain development after birth and stopping development of the body at a stage resembling the juvenile stage in other apes. See Figures 4.17–4.19