We are interested in how cell polarity is controlled during metazoan development. Our approach is to identify and study genes involved in the control of cell polarity by identifying mutations that disrupt the polarities of individual cells. Mutations in
lin-44/Wnt,
lin-17/frizzled and
egl-27/mta1 affect the polarity of certain cells in the tail called TL and TR. We screened for additional mutants that affect T cell polarity to identify new genes that may interact with known genes to control T cell polarity. We have isolated mutations defining two new genes,
tcl-2 and
tlp-1 (T cell lineage defective and T cell lineage and leptoderan tail, respectively). Mutations in
tcl-2 and
tlp-1 are recessive. Cell lineage analysis revealed that both
tcl-2 and
tlp-1 mutations cause defects in T cell division patterns consistent with defects with cell polarity. In addition,
tcl-2 and
tlp-1 males have abnormal tails. In particular,
tlp-1 males have tail morphologies reminiscent of Leptoderan nematode species. Transformation with T23G4 and a 10 kb genomic fragment containing T23G4.1 rescued the
tlp-1 phasmid dye-filling defect. In addition we found sequence changes in
tlp-1 mutants in T23G4.1:
tlp-1(
bx85) contains a 5 base-pair deletion resulting in frame shift and early stop codon and
tlp-1(
mh17) is a nonsense mutation. T23G4.1 encodes a protein with weak similarity to NocA which is required for the embryonic brain and the adult ocellar development in Drosophila (Cheah et al., 1994, Mol Cell Biol., 14:1487-1499). A transgene in which GFP was fused in frame with TLP-1 rescued the phasmid dye-filling defect and was expressed in the nuclei of the posterior intestine cells, the tail hypodermal cells and the T cells. The pattern of
tlp-1 expression was consistent with the defects we have observed. These results suggest that
tlp-1 encodes a transcription factor required for cell polarity and patterning in the C. elegans tail.