Worm Breeder's Gazette 15(3): e4 (June 1, 1998)

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.

The Roles of egl-20/Wnt and lin-44/Wnt in T cell Polarity

Jennifer Whangbo1, Mike Herman2, Cynthia Kenyon1

1 Department of Biochemistry, University of California-San Francisco, 94143-0554
2 Division of Biology, Kansas State University, Manhattan, KS 66506

        The T seam cell lineage consists of an anterior branch which
generates primarily hypodermal fates and a posterior branch which
generates neuronal fates.  Genes required to properly orient or specify
the asymmetric cell fates in the T lineage include lin-44/Wnt and
lin-17/Fz.  In lin-44 mutants, the polarity of the asymmetric divisions
is reversed such that the anterior branch generates neuronal fates and
the posterior branch generates hypodermal fates.  Mutations in lin-17
prevent the specification of the neuronal fates and as a consequence,
both branches give rise to only hypodermal fates.  Thus, mutations in
lin-44 cause polarity reversals, whereas mutations in lin-17 result in
"symmetric" divisions of the T lineage.  We have previously reported
that polarity of the T seam cell lineage is rendered symmetric in
lin-44(n1792); egl-20(n585) double mutants as in lin-17 single mutants
(1,2).  These data supported the model proposed by Sawa and Horvitz that
two different Wnt signals could act through the lin-17/Fz receptor to
orient the asymmetric T cell divisions (3).  Upon further examination of
the double mutant, we have found that egl-20 does not significantly
influence T polarity in a lin-44 background.
        One possibility for the mis-scoring is that all animals were
staged and scored at the same time after hatching.  However, the lin-44;
egl-20 animals develop slightly slower than wild-type animals or lin-17
and lin-44 single mutants.  Thus, at the time when the T granddaughters
in wild-type animals had unambiguously adopted hypodermal and neural
fates, the T granddaughters in lin-44; egl-20 animals had not completely
differentiated and the neuronal cells were not distinguishable from the
hypodermal cells.  We have repeated the experiment by scoring all
animals at similar developmental timepoints, such as when all P nuclei
have descended into the ventral cord.  To eliminate the possiblity of an
error in strain construction, we have independently re-built and
re-scored the double mutant strain.  In all cases, the lin-44; egl-20
double mutants are not significantly different from lin-44 single
mutants.  The results are shown in Table 1.

1 Whangbo et al., Worm Breeder's Gazette 14:4.
2 Herman et al., 1997 IWM Abs.
3 Sawa et al., Genes and Dev. 10:2189-2197.

Table. 1
                                       Polarity (%) at 20 C 
Genotype                     Wild-type    Reversed     Symmetric    n

N2                              100           0            0        54
lin-44(n1792)                     2          94            4        50
lin-17(n671)                     17          26           57        54
lin-17(n677)                     16           8           76        63
lin-17(n3091)                    11          11           78        37
lin-44(n1792); egl-20(n585)       2          83           15        52