Worm Breeder's Gazette 11(4): 93

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mig-5 Mutations Affect Early Gonadal Cell Fates

Ed Hedgecock

Figure 1

mig-5 is required for determination of distal tip cells (DTCs) in 
both sexes and for their program of migration in hermaphrodites.  In a 
sample of rh94 hermaphrodites (N=119), about 10% (23/238) of the DTCs 
were absent, including 1 sterile individual with no DTC and 2 
individuals with three DTCs.  In rh147 (N=101), about 24% (49/202) of 
the DTCs were absent, including 6 individuals lacking both DTCs.  
These frequencies of double DTC loss, 1% = 10% X 10% and 6% = 24% X 
24%, are consistent with independent behavior of gonadal precursors Z1 
and Z4.  Using the more penetrant allele rh147, we hope to follow an 
aberrant gonadal lineage through the early larval stages.  A simple 
possibility is that presumptive DTCs sometimes become 
sheath/spermathecal precursors like their sister cells; rare extra 
DTCs in rh94 could reflect a converse transformation.  Conceivably, 
null mutants of this gene may make no DTCs.  Although some rh94 and 
rh147 males have normal gonads; most lack a functional DTC and are 
hence defective in germline proliferation (Glp).  Such sterility is 
much commoner in mig-5 males than hermaphrodites perhaps because DTCs 
arise by a somewhat different lineage in males (Z1.a/Z4.p) than 
hermaphrodites (Z1.aa/Z4.pp)(1).  Sterile mig-5 males often have a 
second linker cell.  In wild type, both Z1.paa and Z4.aaa are 
competent to become linker cells (primary fate) but cell interactions 
divert one cell to a secondary fate (vas deferens precursor).  By 
analogy to the hermaphrodite anchor cell, this interaction may require 
direct cell-cell contact (2).  In mig-5, the pattern of cell contacts 
may be perturbed, allowing both cells to become linker cells.  
Invariably, one linker cell has a normal trajectory but the second 
cell may migrate less completely (Figure 1).  In hermaphrodites, 
distal tip cells (DTCs) migrate from ventral to dorsal body muscles 
during L3 lethargus.  In some mutants, dorsal movement occurs 
precociously (dpy-24) or fails entirely (mig-7, 
rors give a distinctive gonadal shape that is 
recognized at low magnification with bright field optics.  In rh94, 5-
10% of DTCs execute their dorsal movement during L2 lethargus, i.e., a 
full larval stage early (Figure 2).
Eight known genes (emb (e1933; III), hch-1(X), mab-5(III), mar(rh148;
X), mig-1(I), mig-5(II), mup(rh80;X),and unc-40(I)) are required for 
the posterior migration of neuroblasts QLa and QLp during the first 
larval stage (2,3; unpublished data).  Each of these mutants has 
unique, additional phenotypes, e.g., hch-1 affects secretion of a 
protease used for digesting the eggshell.  emb(e1933) and mig-5 have 
strong maternal effects: emb+ expression is sufficient for 
embryogenesis but not larval Q migrations while maternal mig-5+ 
expression is sufficient for larval cell lineages including Q 
migrations.  For most of these mutants, including mig-5 (rh94), the 
QLa/QLp defect but not other phenes, is suppressed in doubles with the 
semidominant mutation e1751 causing posterior migration of neuroblasts 
QRa/QRp when alone.
The major changes in cell direction during gonadal cell migrations 
may be caused by intrinsic changes within the migrating cells (E.  
Hedgecock, D.  Hall, J.  Culotti, in preparation).  In this view, the 
evolving trajectory reflects progressive differentiation of the motile 
cells.  Mutations affecting the Q lineage/migration suggest a slightly 
different emphasis; here, changes in cell direction coincide with cell 
divisions and determination of new cell types.  By analogy, gonadal 
migrations may be regarded as degenerate cell lineages with periodic 
changes in cell direction (alias type) but no actual divisions.  mig-5 
affects various cell fates in the larval gonad and hypodermis; like 
mab-5, it may be affecting cell migrations indirectly by regulating 
genes involved in cell adhesion and guidance (4,5).
[See Figure 1]

Figure 1