Asymmetric cell division is a fundamental mechanism to produce cellular diversity during development. To divide asymmetrically, mother cells must have polarities. In C. elegans , polarities of mother cells are often regulated by wnt genes. In early development, a polarity of the EMS blastmere is regulated by
mom-2/wnt (1, 2). During postembryonic development, polarities of V5 and T cells are regulated by
egl-20/wnt and
lin-44/wnt , respectively (3, 4). In
egl-20 and
lin-44 mutants, polarities of the V5 and T cell divisions, respectively, are often reversed.
egl-20 and
lin-44 are expressed posteriorly to their target cells (4, 5). We have previously proposed that LIN-44 activates LIN-17/Frizzled receptor at the posterior but not anterior side of the T cell to give them a posterior directed polarity (6). The polarity reversal phenotype in
lin-44 mutants could be caused by an unidentified signal (wnt?) expressed anteriorly to the T cell. If the hypothesis is correct, posterior expression of wnt must be important. However, Whangbo et al. showed that ectopic expression of
egl-20 in pharynx can rescue the polarity reversal of V5 in
egl-20 mutants, suggesting that
egl-20 has only permissive roles in the regulation of the V5 cell polarity (3). To examine this is also the case for
lin-44 , we expressed
lin-44 similarly in pharynx using the
myo-2 promoter to find that it did not affect the T cell phenotype in
lin-44 mutants. Because pharynx may be too far from the T cell, we next expressed
lin-44 just anterior to the T cell using the
egl-5 promoter (expressed in cells around the rectum). Surprisingly, the polarity reversal phenotype in
lin-44 mutants was enhanced from 71% to 97 % by the
egl-5::
lin-44 transgene. The results show that the T cell can recognize direction of the LIN-44 signal, and strongly suggest that LIN-44 instructs direction of cell polarity. (1) Thorpe et al. Cell 90 , 695-705 (1997). (2) Rocheleau et al. Cell 90 , 707-16 (1997). (3) Whangbo et al. Development 127 , 4587-98 (2000) (4) Herman et al. Cell 83 , 101-110 (1995). (5) Whangbo & Kenyon , Mol Cell 4 , 851-855 (1999). (6) Sawa et al. Genes Dev 10 , 2189-2197 (1996).