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Fig. 6. A model for the functions of vhnf1 and val in directing
hindbrain development. RA activates hoxb1b and hoxb1a
expression to initiate an r4 development program, including the specification
of Mauthner neurons. An unknown factor, `X', initially represses
hoxb1a in r5 and r6, independent of vhnf1. RA activates
vhnf1 expression, which reinforces repression of hoxb1a
expression in r5 and r6, possibly in cooperation with an unknown co-factor,
which may or may not be the same `X' above. Repression of hoxb1a by
Vhnf1 blocks acquisition of r4 neuronal fates in r5 and r6, but Vhnf1 must act
through Val to drive r5-6 neuronal development, including abducens cranial
motor neurons (CMNs). Furthermore, Val is required for the acquisition of r5-6
cell-surface characteristics by both activating r5-6 EphB4a
expression and repressing r4-like ephrin-B2a expression in r5 and r6.
Finally, Val contributes to the maintenance of hoxb1a repression at
later stages, possibly through activation of hox group 3 genes.
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