lin-29 males are mating defective and their body hypodermal seam cells fail to terminally differentiate. We were curious whether or not the mating defect reflects a non-hypodermal requirement for
lin-29. Phenotypic analysis of
lin-29 mutant males revealed short spicules in all
lin-29 mutants examined. We then asked which nuclei in
him-5 males accumulate LIN-29. The first male-specific accumulation of LIN-29 is in the linker cell at the L3 stage. In the late L3, approximately 8 nuclei in the spicule/anal region accumulate LIN-29. By the late L4, this number increases to approximately 16 nuclei in the spicule/anal region, 5-7 nuclei in the pre-anal ganglion, and 4 nuclei in the tail tip (post-anal) region. The B cell is in part responsible for LIN-29 accumulation in the spicule/anal region, since B kills greatly reduced the number of staining nuclei. In addition, LIN-29 accumulation patterns in
lin-17 (B.p to B.a transformation) and
vab-3 (B.a to B.p) mutants suggest that many of the LIN-29 accumulating cells are B.a descendants. Despite the spicule defect and B cell staining patterns, we have not observed B cell lineage defects these animals. In adult males additional ventral cord nuclei accumulate LIN-29. These nuclei have been tentatively identified as VA and DA motorneurons by co-staining
unc-4::lacZ integrants (D. Miller) with antibodies to LIN-29 and beta-gal. Other male specific blast cell progeny may also accumulate LIN-29. We have rescued the
lin-29 male mating defect with a transgene and will use mosaic analysis to identify the cells in which
lin-29 is required for proper spicule length and mating. Since spicule cells (all B.a derived) produce cuticle1 and LIN-29 is a transcription factor which regulates certain stage-specific collagens2, one possibility is that LIN-29 regulates the transcription of particular collagen genes required during spicule development. 1Sulston, Albertson and Thomson (1980) Dev. Biol. 78:542-576 2Rougvie and Ambros (1995) Development 121:2491-2500.