Worm Breeder's Gazette 10(3): 122

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.

Body Wall Contacts Help Arrange the Hermaphrodite Gonad Primordium

E. Hedgecock, J. Culotti and D. Hall

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The embryonic gonad comprises four cells pressed against the ventral 
body wall (Fig.  1).  Cell divisions in the first larval stage create 
2 distal tip cells (DTC), 4 sheath/spermathecal (SS), 2 dorsal uterine 
(DU), and 4 ventral uterine (VU) precursors plus mitotic germ cells (
Fig.  2).  The somatic cells, excepting the distal tip cells, coalesce 
during the second larval stage, displacing all germ cells from the 
central region of the gonad.  The 6 uterine cells form a central prism 
with the 4 VU cells contacting the body wall and 2 DU cells facing the 
body cavity.  The fates of the four ventral uterine cells are 
regulated by interactions between the uterine cells or their immediate 
descendants.  Most strikingly, either Z1.ppp or Z4.aaa, becomes the 
unique anchor cell, the primary fate for this pair of equivalent cells.
The committed anchor cell moves to the center of the ventral uterus 
and induces vulval development (Fig.  3).
Division axes and early movements of gonadal cells may be determined 
by affinities between gonadal cells and by affinities of specific 
somatic cells, e.g., distal tip cells, for the body wall.  Here we 
report that unc-6 and unc-40 mutations disturb the arrangement of the 
hermaphrodite gonad primordium perhaps by disrupting adhesion of VU 
cells, including the anchor cell, to the epidermis.
unc-6 and unc-40 hermaphrodites are often absolutely defective in 
egg-laying (see Fig. 4).  We examined late third stage larvae by DIC 
microscopy.  In about 20% of the animals, the anchor cell was 
displaced laterally or dorsally in uterus and failed to connect to the 
developing vulva.  Such animals were incapable of laying eggs as 
adults.  In another 5-10% of the larvae, 2 anchor cells were present, 
often widely separated on the uterine circumference.  We examined 
early third stage larvae to learn how these anchor cell displacements 
or duplications arise.  The arrangement of the somatic primordium was 
disturbed in many individuals.  Most cell-cell contacts within the 
somatic primordium were preserved in these mutants.  In particular, SS-
DU, DU-DU, and DU-VU contacts appeared to be normal.  The relative 
positions of the 4 VU cells, however, or their relation to the body 
wall, were frequently abnormal.  In particular, left and right VU 
cells sometimes failed entirely to meet each other.  (Two anchor cells 
were formed in these animals suggesting that the regulative 
interaction between Z1.ppp and Z4.aaa mediated by the lin-12 protein 
requires close proximity or direct cell contact.)  In many individuals,
the VU cells were displaced from the epidermis by germ cells (Fig.  4)
.  We have not yet examined younger larvae to learn whether these 
abnormal cell arrangements arise from altered L1 division axes or 
failed L2 cell movements.
A simple model to account for these observations is that VU cells 
adhere to the underlying ventral epidermis.  This adhesion brings or 
holds the left and right VU cells together at the ventral midline, 
establishes the dorsal/ventral orientation of the uterus relative to 
the body wall, and enables the uterine cells to squeeze germ cells out 
of the central region of the gonad.  In unc-6 and unc-40 mutants, this 
adhesion is defective and the uterine cells can be pried from the body 
wall by intruding germ cell.  This model is consistent with 
observations that these genes may guide other ventralward cell 
movements on the body wall.

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