|
|
|
|
|
|
|
||||
| Home Help Feedback Subscriptions Archive Search Table of Contents | ||||
|
Fig. 1. The ASER versus ASEL fate decision in wild-type and lsy-2 mutant
animals. (A) Schematic representation of the bilaterally symmetric ASE
gustatory neurons. Their bilaterality extends to cell position, axonal and
dendritic morphology, synaptic connectivity
(White et al., 1986) and the
expression of a large number of bilaterally expressed genes
(www.wormbase.org).
The enlarged images illustrate the fate differences between ASEL and ASER, and
provide a summary of the genetic regulatory network that controls the ASEL and
ASER fates (Chang et al., 2004;
Chang et al., 2003;
Hobert et al., 1999;
Johnston and Hobert, 2003;
Johnston et al., 2005). The
permissively acting factors lin-49, unc-37 and ceh-36 are
not shown but are referred to in the Discussion. (B) In lsy-2 mutant
animals, ASEL-specific expression of gcy-7, assayed using a
gcy-7prom::gfp transgene (otIs3), is lost and
ASER-specific expression of gcy-5, assayed with a
gcy-5prom::gfp transgene (ntIs1), is derepressed in ASEL.
lsy-2(ot64) null mutant animals are shown. See
Table 1 for quantification of
the data and more alleles.
|
