Worm Breeder's Gazette 11(4): 100

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A Role for lin-32 in Deciding Lateral Hypodermal as well as Neuronal Cell Fates

Connie Zhao and Scott W. Emmons

Two alleles of the gene lin-32, e1926 and u282, have been isolated 
by Kenyon and Hedgecock (1) and Chalfie and Au (2) respectively.  
Recently, another allele of lin-32, bx46, was isolated in our lab in a 
screen for Mab (male abnormal) mutations.  The phenotype of a lin-32 
mutant is loss of both V-rays and T-rays in the male.  We do not 
believe any of the three alleles of lin-32 is a null, because none are 
completely expressive and because strong alleles of lin-32, which are 
also touch insensitive, are rare (2).   lin-32(u282) is the strongest 
allele: about 90% of the males lack all the rays.  We plan to isolate 
more alleles of lin-32 by a non-complementation screen in order to 
determine the null phenotype .
Lineage analysis has been done on lin-32(e1926) by Kenyon and 
Hedgecock (1).  They found that lin-32(e1926) caused the Q, postdeirid,
and ray neuroblast cells to adopt certain hypodermal fates and 
suggested that lin-32 functioned in a switch between certain 
hypodermal and neuronal cell fates.  Mutation in the gene lin-22 has 
the opposite effect (3).  In males, it causes certain hypodermal cells 
to adopt neuroblast cell fates and produce ectopic postdeirids and 
rays.  Rays arise from expression of the ray sublineage, and the 
posterior daughter of the ray precursor cell, Rn.p, does not make alae.
Hence, lin-22 males lack alae.   We constructed a lin-22(mu2);lin-32(
u282) double mutant and found that, in double mutant males, lin-32 was 
epistatic to lin-22 in blocking the formation of ectopic postdeirids 
and rays, as pointed out previously by Kenyon and Hedgecock (1).  
Therefore, lin-32 appears to act downstream of lin-22 in generation of 
a neuroblast.  If the lin-32 mutation only affected neuroblast cell 
fates, then we would expect to find neither rays nor alae in the lin-
22; utant.  But interestingly, we found 
almost intact alae in double mutant males except at two or three 
broken points.  One explanation for this phenotype is that the lin-32 
mutation may not only affect neuroblast cell fates, but also certain 
hypodermal cell fates; it may transform the ectopic Rn.p cells 
produced in the lin-22 mutant from non-alae producing cells (tail seam 
cells?) into body seam cells.  This effect of the lin-32 mutation in 
the lin-22 background is in contrast to its effect as a single mutant, 
where it does not affect hypodermal fates (lin-32 males do not have 
posterior alae, implying that Rn.p cells are not transformed to body 
seam cells).  Alternatively, one or both of the daughter cells of Rn.a 
in lin-22;lin-32 double mutant may be transformed into body seam cells 
and produce alae.  We are now following the cell divisions in the 
double mutant to characterize it further.  We thank Duc Nguyen for 
isolating the bx46 allele.