Worm Breeder's Gazette 10(1): 111

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.

pal-2(e2260), a Mutation Transforming Tail Seam to Body Seam

M.M. Shen

The EMS-induced mutation pal-2(e2260), isolated in a screen for 
abnormal male mutations, causes the production of ectopic Posterior 
Alae in the tail region of mutant males, where normally no alae are 
present.  Unlike other mutations which cause a similar Pal phenotype, 
such as mutations in mab-3 or mab-5, 60) males 
possess the full complement of rays.  These rays, however, are 
somewhat abnormal in appearance, implying a morphogenetic defect; pal-
2(e2260) males mate poorly.  Otherwise, pal-2 males appear completely 
wild-type, as do pal-2 hermaphrodites.  pal-2 maps very close to fem-3 
on linkage group IV, and is covered by eDf18 and eDf19.  For both 
deficiencies, deficiency heterozygote males appear identical in 
terminal phenotype to e2260 homozygotes, showing that e2260 is a 
reduction- or loss-of-function allele.  Towards the end of the L4 
stage in wild-type males, 'tail seam' activity, which does not lead to 
alae formation, is produced by the ray precursor posterior daughters 
R1.p through R5.p.  Lineage analysis of pal-2(e2260) males indicates 
that the ray precursor cell divisions, as well as nuclear positions, 
are essentially wild-type (5 sides examined).  However, R1-5.p have 
characteristics of the alae-producing body seam, allowing alae 
formation to extend ventro-posteriorly to the fan, around ray 1, with 
alae-like dots then continuing dorso-posteriorly up the fan.  R1.p and 
R2.p clearly participate in alae formation, being located in the body 
seam band, while R3.p, R4.p, and R5.p, which still seem to be part of 
a tail-seam-like bag, appear to be responsible for the alae-like dots. 
The anterior movement of the R1-5.p nuclei during L4 lethargus occurs 
normally.  Thus, it appears that pal-2(e2260) males may retain partial 
tail seam function.  This interpretation is consistent with the 
staining pattern observed with a monoclonal antibody, NE2/1B4-14, 
isolated in an unrelated study (H.  Schnabel, J.  Priess, S.  Green, 
and T.  Lowe, personal communication), which appears to recognize a 
cuticular product of seam cells that do not form adult alae.  This 
antibody stains in a thin fibrous band laterally along the body of 
late embryos and wild-type larvae of both sexes (many larvae do not 
stain, indicating a correlation with seam activity), but not adult 
hermaphrodites.  Wild-type adult males stain in a band approximately 
where the tail seam is located in the L4 stage, starting laterally 
slightly anterior to the tail, and continuing posteriorly where the 
fan attaches to the body.  pal-2(e2260) adult males display greatly 
reduced staining, with the anterior part of the lateral band 
eliminated.  Two explanations could account for the phenotype of e2260 
males.  It might be that incorrect tail morphogenesis causes the Rn.p 
cells to join the body seam inadvertently, or it might be that the Rn.
p cells are transformed in cell fate, with a secondary effect on ray 
morphogenesis.  The study of double mutants supports the latter 
possibility.  The mutation lin-22(n372) causes V1-V4 to be transformed 
into a V5-like lineage, thus resulting in the production of ectopic 
ray precursor cells in mutant males (Fixsen and Horvitz, WBG 7 #2: 40).
Consequently, lin-22 males produce only 10% of wild-type alae on 
average, as measured in relative fraction of body-length.  The double 
mutant lin-22 owever, produce 56% of wild-
type alae in body-length (more than 30 animals of each genotype 
examined).  Many of these animals can be seen to have ectopic ray 
papillae in the midst of stretches of wild-type alae; occasionally, 
round knobs of sclerotic material are also present, possibly resulting 
from cuticular confusion.  A similar suppression effect can be 
observed in double mutants with lin-32(e1926) males (Kenyon and 
Hedgecock, WBG 8 #2: 19), which frequently possess a gap in their alae 
around the postdeirid region (17/41 sides examined); the lineage basis 
for this phenotype is not known.  In pal-2(e2260); 
926) males this alae defect is completely 
suppressed (32/32 sides).  It therefore appears that pal-2 is a gene 
involved in the specification of a differentiated cell fate.  Like 
other genes involved in generating sexual dimorphism in the male 
lateral hypodermis (see WBG 9 #3: 96), a mutation in pal-2 causes a 
transformation towards the formation of body seam.  Finally, the 
phenotype of pal-2(e2260) is additional evidence that the tail seam 
plays a relatively minor role in male tail morphogenesis, consistent 
with the laser ablation experiments of Sulston et al.  (Dev.  Biol.  
78: 542 (1981)).