Chapter 7 Summary


  1. Apoptosis sculpts body parts by removing adjacent structures, such as the webbing between digits. See Figure 7.1
  2. Neuronal apoptosis serves to regulate the number of neurons to match the need, as the number of motor neurons in each segment of the spinal cord is appropriate for the number of muscles that need innervation. See Figure 7.2
  3. In the final hours of apoptosis, dying cells take on a characteristic pyknotic profile. While few pyknotic cells are visible at any single point in development, their peak matches the time when spinal motor neurons go missing, confirming that the motor neurons have indeed died rather than migrating away or differentiating into some other type of cell. See Figures 7.3–7.5
  4. Introducing mouse tumor cell lines next to chick embryos uncovered a protein that prevents apoptosis of dorsal root ganglion (DRG) cells and sympathetic ganglia cells. This nerve growth factor (NGF) has both tropic and trophic effects on these types of neurons, but little or no effect on others. See Figures 7.6–7.9
  5. When NGF contacts a responsive neuron, it is internalized and retrogradely transported to the cell body, where it regulates gene expression, which can forestall apoptosis and encourage process outgrowth. See Figure 7.10
  6. NGF is part of a family of neurotrophins, which includes brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), and NT-4, which bind with high affinity to the Trk family of receptors as well as the low-affinity p75 receptor. See Figures 7.11–7.13, Table 7.1
  7. There are other neurotrophic factors in addition to the neurotrophins, including ciliary neurotrophic factor (CNTF) and glial cell line–derived neurotrophic factor (GDNF).
  8. Experiments in C. elegans proved that apoptosis was an active process, and not the result of attack from immune system cells that clean up debris. They also revealed the importance of death genes, including those for caspases, which the cell produces to dismantle itself. We can exploit the fragmentation of DNA by TUNEL labeling to detect dying cells even before they become pyknotic. See Figure 7.14
  9. The main molecular pathway for apoptosis is basically the same in worms and vertebrates, but the latter species have more molecular players, such as Diablo and inhibitors of apoptosis proteins (IAPs). These additional regulatory pathways provide a system of checks and balances to determine the cell’s survival. See Figures 7.15 and 7.16
  10. We still don’t know which cells initially die in ALS, but in those few cases that have a genetic basis, animal studies indicate that the motor neurons themselves are not the site of action.
  11. In vertebrates, the same testicular hormones that masculinize the body also exert an organizational effect on the developing nervous system to masculinize it. Androgens such as testosterone either forestall neuronal apoptosis to provide adult males with more neurons, as in the SDN-POA, or augment apoptosis to leave males with fewer neurons, as in the AVPV. See Figures 7.21–7.26
  12. In rodents, androgens act on developing bulbocavernosus muscles to preserve them, and thereby preserve their motor neurons in the spinal nucleus of the bulbocavernosus (SNB). See Figures 7.27 and 7.28
  13. In flies, a cascade of transcription factors, starting with sex-lethal (Sxl) on the X chromosome, directs sexual differentiation of each part of the body in a cell-autonomous fashion. Several genes downstream from Sxl is fruitless (fru), a transcription factor gene that is translated only in male flies because the only transcripts of fru produced in females are nonfunctional. See Figure 7.29
  14. In male flies, expression of fru prevents apoptosis of a network of neurons that mediate male courtship behavior. Thus expression of male-specific transcripts of fru is both necessary and sufficient to produce male courtship. See Figures 7.30–7.32
  15. In humans, there is evidence that prenatal androgens may predispose individuals to be sexually attracted to females—body markers indicate that lesbians, on average, were exposed to more prenatal androgens than straight women. There is no evidence that gay men were exposed to less prenatal androgen than straight men, but the fraternal birth order effect demonstrates that there are prenatal influences on sexual orientation in men, too. See Figures 7.33 and 7.34