Worm Breeder's Gazette 9(2): 62

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.

Lineage Alterations in mab-3 Mutants

M. Shen

Figure 1

Mutations in the gene mab-3 cause a variety of male-specific defects.
mab-3 males lack most of their rays, possess a greatly diminished 
fan, and produce large quantities of yolk proteins (see 1985 CSH C.  
elegans Meeting Abstracts, p.  129), while mab-3 hermaphrodites appear 
wild-type.  An examination of terminal phenotypes of mab-3 males 
suggested possible defects in the lateral hypodermal lineages (and 
perhaps in the B lineage), but probably not in the germline (WBG 9 #1: 
87) or ventral hypodermis.  All of these structures appear normal in 
mab-3 hermaphrodites.
I have followed the lineages of the lateral hypodermal blast cells 
V5, V6, and T from mid-L2 to late L4 in mab-3(e1240) males.  (e1240 is 
a candidate for a null mutation, as its terminal phenotype seems 
identical to that of e1240/Df, using deficiencies that span the mab-3 
locus.  The lineage alterations in the mab-3 male lateral hypodermis 
appear to be confined to the nine ray precursor (Rn) sublineages that 
generate nine ray cell groups (R1 descends from VS, R2-6 from V6, and 
R7-9 from T).  The mutant lineage that mab-3 ray precursors can follow 
is depicted in the figure below, along with the wild-type ray 
precursor lineage.  In mab-3(e1240) males, R1-4 generally adopt the 
mutant lineage, while R7-9 usually remain wild-type, and RS and R6 
often follow an intermediate lineage.  These results are consistent 
with the terminal phenotype.  The anterior-posterior distribution of 
mutant lineages may reflect a gradation in the requirement for mab-3 
gene product; this distribution is also observed in the terminal 
phenotypes of two weaker mab-3 alleles, e1921 and e2093.
I have begun to examine the effect of mab-3(e1240) in combination 
with mutations that create ectopic ray cell groups.  For example, 
males of lin-22(n372) (isolated by Bill Fixsen; see WBG 7 #2: 40) form 
an ectopic postdeirid and a pair of ectopic rays from each of V1-V4.  
mab-3;lin-22 males produce ectopic postdeirids, but instead of 
producing ectopic rays, they generate alae (based on inspection of 
late L4 animals).  Thus, it appears that mab-3 mutations are capable 
of creating a transformation from ray to seam cell fates.  This is 
reasonably consistent with the mab-3(e1240) terminal phenotype, in 
which patches of abnormal alae-like structures are seen in the tail 
region, where normally no alae are found.
[See Figure 1]

Figure 1