The seam cells are a distinct group of hypodermal cells that generate a variety of cell types during postembryonic development. We are interested in what mechanisms make the seam cells different from their hypodermal neighbours. Previous work has indicated that
lin-1 mutants exhibit defects in the development of the V1 cells (1). We have extended this initial observation to determine the role of LIN-1 in V1 cell fate and investigated how LIN-1 function is regulated in the development of these cells. In
lin-1 null mutants V1 cells adopt an aberrant, rounded cell morphology, and their apical surfaces are much reduced compared to wild-type. In postembryonic development V1 frequently fails to divide further, and when it is seen to divide it fails to execute a normal seam cell lineage. These observations suggest that
lin-1 is required to specify seam cell fate in V1 cells. Consistent with this hypothesis, none of the seam cell markers that we have examined are expressed in V1 cells in
lin-1 mutants, although the epidermal marker, LIN-26, is still expressed, suggesting that these transformed cells have retained epidermal characteristics. Using the knowledge of how LIN-1 is regulated in the developing vulva we have investigated to what extent this regulation is conserved in V1 cell development. This work has revealed that as in vulval development, LET-60 regulates LIN-1 activity through the MAP kinase cascade encoded by
sur-1/mpk-1 and
mek-2. However, the upstream components of the vulval pathway do not appear to be present in V1 cell development. We can find no evidence that the synMuv gene products play any role in V1 cell fate, nor does LET-23 appear to regulate the activity of the pathway. We are currently carrying out genetic screens to attempt to identify how LET-60 activity, and thus LIN-1 activity, is regulated during V1 cell development. One curious feature of this work is the fact that the fates of the other seam cells are not appreciably perturbed by the loss of
lin-1 function. In particular, V2, V3 and V4, which have identical cell fates to V1, develop normally throughout embryonic development. We have investigated whether the source of this apparent difference might lie in the differential expression of the Hox gene
lin-39, which is expressed in V2-4 but not V1, but found no evidence for this hypothesis. It may be that other genes compensate for the lack of
lin-1 expression in V2-4, or perhaps
lin-1 is not involved in seam cell fate in these cells. 1) Sulston and Horvitz (1981). Dev. Biol. 82, 41-55.