Worm Breeder's Gazette 10(2): 110

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.

Q Neuroblast Migration in lin-21/mab-5 and lin21/nDf16 Heterozygotes

S.J. Salser and C. Kenyon

Figure 1

QL and QR are generated through identical patterns of division from 
ABpl and ABpr, and they divide identically, to produce three neurons 
and two programmed cell deaths.  Yet QL descendants stay near V5.a or 
migrate back into the tail, while QR and its descendants migrate 
anteriorly past the gonad into the vicinity of V2.a or the head.  Five 
genes are known to influence the direction of migration of these 
neuroblasts.  Recessive mutations in the genes mab-5, 
3), and hch-1 cause both QL and QR to migrate 
anteriorly, while a semidominant mutation in the gene lin-21 prevents 
QR and its descendants from migrating past the gonad.
There are three reasons to suspect that lin-21(e1751) might be a 
gain of function allele of mab-5.  First, e1751 has the opposite 
effect on Q migration.  Second, mab-5 and lin-21 have not been 
separated in mapping experiments.  16 recombination events between dpy-
17(e164) and unc-32(e189) failed to separate mab-5(e1239) and lin-21(
e1751) (E.  Hedgecock, personal communication).  Third, a restriction 
fragment length polymorphism associated with e1751 has been seen on 
two Southern blots probed with putative mab-5 DNA sequences.  (R.  
Hoskins, MRC pers.  comm., repeated by M.  Costa, UCSF)
If mab-5(e1239) is a null allele of lin-21, then it should behave 
like a deficiency when in trans to e1751.  Otherwise, since known mab-
5 alleles are recessive, e1751/e1239 should resemble e1751/+.  Here 
are the positions of Q descendents in L2 heterozygotes.  There were 
regularly two Q descendants in the body region 
[See Figure 1]
First, since e1751/nDf16= e1751/e1751, e1751/+, e1751 is likely to 
be a neomorphic mutation whose effects on Q migration can be 
alleviated by wild type gene activity.  Second, the phenotype of 
e1751/e1239 resembles that of e1751/+, while the phenotype of 
e1751/nDf16 is quite different, and resembles the e1751/e1751 
phenotype.  This suggests, as argued above, that e1751 is not an 
allele of mab-5.  However, it is always possible that e1239, while 
null for the mab-5 wild-type activities, retains activity in 
suppressing e1751.  Examination of more mab-5 alleles over e1751 will 
help rule out this possibility.

Figure 1