Info

r1 r2 r3 r4 r5

EphA2

r1 r2 r3 r4 r5

FasII

Hoxb1 Hoxa1

EphA2

Figure 4 Comparable brain phenotypes in lab/Hox1 loss-of-function mutants in Drosophila and mouse. (Left) Simplified scheme of the deutocerebral (b2), tritocerebral (b3), and mandibular (s1) neuromeres of the Drosophila brain. In the wild type (wt) cells in the posterior tritocerebrum express lab (blue) and also express the neuron-specific marker ELAV and the cell adhesion molecule FaslI. In the lab null mutant (lab~'~), cells in the mutant domain are present but do not extend axons and fail to express the neuron-specific marker ELAV and the cell adhesion molecule Fasll, indicating a total loss of neuronal identity. Axons from other parts of the brain avoid the mutant domain. (Right) Simplified scheme of rhombomeres r1-r5 of the mouse hindbrain. In the wild type (wt) cells in r4 co-express Hoxal and Hoxbl and also express the r4-specific marker EphA2. In the Hoxa1~'~; Hoxb1~'~ double homozygous mutant, cells in r4 are present but the r4-specific marker EphA2 fails to be activated in r4, indicating the presence of a territory between r3 and r5 with an unknown identity. The double mutant also exhibits multiple defects in the motor neuron axonal projections; facial motor neurons are scarce and exit randomly from the neural tube. Reproduced from Hirth, F. and Reichert, H. 1999. Conserved genetic programs in insect and mammalian brain development. Bioessays 21, 677-684, with permission from John Wiley & Sons, Inc.

Was this article helpful?

0 0

Post a comment