Worm Breeder's Gazette 11(5): 84

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.

egl-20: A Gene Which Determines Both the Extent and Direction of Migration of the Q Descendents

Jeanne Harris, Monica Gerber and Cynthia Kenyon

Figure 1

egl-20 initially caught our interest because reduction- or loss-of-
function mutations in this gene have two effects on Q cell migration.  
The most striking Q defect in egl-20 mutants is that the daughters of 
QL migrate anteriorly, as they do in mab-5(lf) mutants, rather than 
remaining in the posterior, as they do in wild-type worms.  What is 
unusual about egl-20 mutations is that they also affect the distance 
the Q descendents migrate anteriorly: in egl-20 mutants the Q 
descendents Q.paa and Q.pap stop short of their final destination.
Genetic and molecular epistasis suggests that the reason the QL.x (i.
e.  QL.a and QL.p) cells migrate anteriorly in egl-20 mutants instead 
of remaining in the posterior is because they fail to turn on mab-5.  
First we found that the mab-5(gf) mutation could suppress the egl-20 Q 
defect.  When the mab-5(e1751gf) mutation is introduced into an egl-20 
strain the QL and QR descendents migrate posteriorly.  This suggests 
that egl-20 could act upstream of mab-5 in determining the direction 
of migration of Q descendants.
By examining the pattern of  -gal activity in egl-20(n585) mutants 
carrying an integrated mab-5::lacZ reporter construct (Salser and 
Kenyon, this WBG) we were able to ask whether egl-20 mutations affect 
mab-5 gene expression.  In a wild-type background QL.x cells stained 
dark blue 3-4 hrs after hatching in 47/50 worms examined whereas QR.x 
cells never stained (0/50).  In egl-20(n585) mutants carrying the 
construct, however, QL.x were never observed to stain (0/43).
egl-20 mutations do not affect most of the other structures the 
require mab-5 activity.  Consistent with this, the mab-5-lacZ L1 
staining pattern did not differ markedly from wildtype, although this 
has not yet been carefully quantitated.
Together these data suggest that egl-20+ is required for mab-5 gene 
expression in QL.x cells and that QL's descendents migrate anteriorly 
in egl-20 mutants because they fail to turn on mab-5.The second 
alteration in egl-20 mutants is a displacement of the Q.paa and Q.pap (
SDQ and AVM/PVM cells).  On both sides of egl-20 mutants, these cells 
are positioned further posteriorly than the normal positions of SDQR 
and AVM.  An additional observation suggests that this alteration is 
due to an altered signal to stop migrating rather than a simple 
inability to migrate.  In the mab-5(e1751gf);egl-20(n585) double 
mutant which 'rescues' the QL.x cells and allows them to remain in the 
posterior, there is a different type of misplacement: this time the Q 
descendents often migrate too far posteriorly (compared to e1751 alone)
How can we explain the two different effects egl-20 mutations have 
on the migration of the Q descendents?
Possible models which explain the two effects of egl-20:1) 2 
separate problems: egl-20 has one activity needed to determine the 
direction of migration of the Q descendents and another needed for the 
Q descendents to stop in the right place.  It could do this in many 
ways (interacting with two different proteins, DNA sites, etc., by 
being present in two forms, one form with two domains, etc....).
2) one underlying problem: a single egl-20-dependent system of 
positional information is used both to stop migrating cells in the 
correct place, and also to turn on mab-5.  In this model, the wild-
type QL cell turns on mab-5 when its initial posterior migration 
brings it in contact with a cell-extrinsic signal located in the 
posterior 'mab-5 domain'.  In egl-20 mutants this positional 
information is shifted posteriorly relative to the Q cells, which 
prevents QL.x cells from receiving their positional cue to turn on mab-
5.  Because mab-5 is not turned on, the QL daughters migrate 
anteriorly.  Similarly, when the anterior Q descendents stop short of 
their full anterior position, it is because the signals to stop 
migrating are also shifted posteriorly relative to the Q-descendants.  
In the mab-5(gf);egl-20 double mutant, the extreme posterior 
displacement of Q.pap and Q.paa can be explained if they too are 
seeking out their 'proper' final location which the egl-20 mutation 
has shifted more posterior relative to the rest of the worm.  Because 
mab-5 has been turned on independently of egl-20 by the e1751gf 
mutation, the cells are able to stay in the posterior region and 
locate their egl-20-directed final position.  A final attractive 
feature of this model is that it can also accomodate another egl-20 
phenotype; namely, altered HSN migration.  Like the Q descendants, the 
HSN cell body is also mispositioned posteriorly in egl-20 mutants (
Trent et al.  Genetics 104:619-647,1983; Desai et al.  Nature 365:638 
646, 1988).

Figure 1