We describe the function of the
lim-6 homeobox gene and compare its mutant phenotype to those of other LIM homeobox genes in the worm.
lim-6, the worm ortholog of the vertebrate
lmx-1a/b genes, is expressed in several head and tail neurons, the excretory gland cell and the developing uterus. Deletion of most of the coding region of
lim-6 causes defects in the terminal differentiation of
lim-6 expressing cells. In the uterus, a specific type of endothelial cells, the uterine toroid cells display adhesive defects. In the chemosensory neuron ASEL,
lim-6 propagates asymmetric information;
lim-6, which is expressed in ASEL, but not ASER, is required to determine the asymmetric repress expression of the putative sensory receptor
gcy-5 in ASEL. All the neurons that express
lim-6 are generated in
lim-6 mutant animals and adopt several correct terminal differentiation features; yet several
lim-6 expressing GABAergic neurons are functionally defective. Specifically, the ultradian defectation rhythm mediated by the GABAergic AVL and DVB motorneurons is defective and AVL and DVB display axonal defects. We find that expression of
unc-25, the gene necessary for GABA synthesis, is partially dependent on
lim-6. We show a GABAergic input into the dauer program and suggest that
lim-6 is necessary for this input. The comparison of the mutant phenotypes of all the LIM homeobox that we have studied reveals striking similarities. Although the LIM homeobox genes
ttx-3,
lin-11 and
lim-6 are expressed in non-overlapping sets of neurons, the neural phenotypes of loss of each LIM homeobox gene functions reveals a common theme: In each case, the neurons are generated, adopt several terminal differentiation features yet display subtle neurite sprouting defects. This observation suggests that each of the LIM homeobox genes regulates the expression of a similar set of target genes in distinct set of neurons.