Worm Breeder's Gazette 9(2): 76

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.

Embryonic Lethals with Early Defects

R. Schnabel and H. Schnabel

One of the methods to characterize the ts embryonic lethals (see 
previous abstract) is to follow the early cleavages up to the 4 E cell 
stage, i.e.  the onset of gastrulation.  So far, 310 embryos from each 
of 65 mutants have been analyzed.  The following 11 mutants were 
selected as potentially interesting.  All of them are maternal effect 
mutants.  Two mutants show specific lineage defects.  In T39 embryos 
P1 cleaves symmetrically and 15 minutes late.  The P-granules which 
are segregated normally into P1 during the first cleavage are 
distributed randomly into the two P1-daughters during the symmetrical 
cleavage.  This indicates that P1 has lost its identity.  Staining 
with monoclonal antibodies specific for MS and E cell descendants 
suggests that P1 has acquired the fate of EMS.  Three further alleles 
were isolated by noncomplementation screening.  Two of these are ts 
and affect the cleavages of P2 and P3, respectively.  In these mutants,
P2 or P3 cleave symmetrically and fail to segregate the P-granules.  
In all alleles, cleavages in the AB lineage are also somewhat slowed 
down.  The terminal phenotypes of all alleles are embryos arrested 
before morphogenesis.  The new nonconditional allele has not been 
characterized yet.  F80 is a dominant mutant which causes MS and E or 
one of their daughters each to exchange their fates.  Three F80-
revertants were isolated which are candidates for recessive alleles 
Of the dominant mutation and one has been characterized further.  In 
this mutant the cleavage pattern of E is similar to that of MS.  In 
addition, the E cell descendants show no gut differentiation judged by 
the lack of the appearance of rhabditin granules.  F249 often has a 
symmetric first cleavage.  Later on in development the different 
lineages divide more and more synchronously.  The terminal 
differentiation of most cell types including the gut cells is not 
affected.  The mutants F248 and F765 show symmetric cleavages of P1 
and P2 
In the mutant F384 the pronuclei remain in the posterior part of the 
egg and do not rotate which results in an aberrant first cleavage 
similar to that of zyg-9 embryos.  In contrast to zyg-9, the embryo 
develops many differentiated cells.  Some of the embryos have an 
inverted anterior-posterior polarity.  Two mutants show altered 
cleavage directions of P1 (F591) or of EMS and C (F350), respectively. 
The new cleavages occur in a direction orthogonal to that of the 
corresponding wild type cells.
Three mutations F346, F618 and F598 (the latter two are allelic) 
cause a delay of the cleavages of the P cells and their daughters by a 
factor of about 1.5.  The AB cleavage rate is not affected.  In the 
mutant F598, P granules are not segregated properly in the late P