Worm Breeder's Gazette 14(2): 70 (February 1, 1996)
These abstracts should not be cited in bibliographies. Material contained herein should be treated as personal communication and should be cited as such only with the consent of the author.
HHMI and Division of Biology, 156-29 California Institute of Technology Pasadena, CA 91125
lin-11 encodes a LIM domain transcription factor (Freyd et al., 1990) and is required for vulval secondary cells to undergo an asymmetric cell lineage (Ferguson et al, 1987). We suspected a uterine defect because, as discussed in a previous WBG [13(3) p. 100], a lin-11-lacZ is expressed in the pi cells and their progeny. pi cells undergo an asymmetric cell division along a dorsal-ventral axis. However, lin-11 does not appear to be required for this asymmetric cell division: the patterns of cell division were wild type in 4/5 n389 animals lineaged. We therefore examined the diffferentiated cell types produced by the pi cells: the uv1 cells and the utse (Newman, White, and Sternberg, this WBG). The utse results from fusion of a subset of pi progeny with the AC and forms the thin laminar process that constitutes the interface between the L4 uterus and vulva. During L4, the utse nuclei migrate (or are squeezed) distally. In 8/8 N2 animals in which the pi cells were ablated, the AC failed to move from its position dorsal to the vulva and sometimes had a "bloated" appearance consistent with its remaining mononucleate in the absence of the correct fusion partners. A thin planar process was not observed dorsal to the vulva; instead, the tissue was thicker. The relevant lin-11(n389) mutant phenotypes are: 1) A thin planar process is not observed dorsal to the vulva during L4. 2) Nuclear migrations of the pi progeny are variably abnormal (some but not all nuclei failed to migrate properly in 5/5 animals lineaged). This suggests that lin-11 may be required for correct differentiation or attachment of the utse cell rather than for nuclear migrations per se. 3) The AC nucleus did not move in the above animals and sometimes appeared bloated. The abnormal AC morphology can be easily scored by anatomy and is highly penetrant in n389. The lin-11 mutant phenotypes are consistent with a defect in utse differentiation or in some but not all aspects of pi cell differentiation.