Worm Breeder's Gazette 11(3): 64

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mes Update

Beth Capowski, Carol Garvin, Paula Martin and Susan Strome

Figure 1

Figure 2

We have been screening for maternal effect sterile (mes) mutations (
WBG 10(3):101) in an attempt to identify maternally encoded factors 
required for germ line development.  Using an F3 screen for sterile 
animals, we have screened 7200 haploid genomes and identified 8 
alleles.  These fall into five complementation groups (see Table 1) 
and all are strict maternal effect mutations.  We predicted that at 
least two classes of mutations might be identified: 1) mutations in 
genes that encode factors required for the determination, 
establishment or maintenance of the germ line and 2) par-like 
mutations that affect cytoplasmic localization of maternal factors (
Cell 52: 311).  Of the mes loci that have been analyzed, three appear 
to belong to the first class while one may affect partitioning of germ 
line determinants.
[See Figure 1]
mes-1 is likely to affect the cellular partitioning machinery.  All 
four alleles of mes-1 are temperature sensitive and incompletely 
expressed; homozygous mothers produce both sterile and fertile progeny.
In addition, all alleles show some mis-segregation of P granules in 
L1 progeny of homozygous mutant mothers.  This suggests that the mes-1 
gene product is involved in a temperature-sensitive process that 
affects partitioning of cytoplasmic components.  However, mes-1, 
unlike previously described partitioning mutations, has fairly low 
embryonic lethality.
[See Figure 2]
mes-2, mes-3 and mes-1 may affect germ-line-specific factors.  The 
remaining three complementation groups show normal P-granule 
segregation to Z2 and Z3 in L1 offspring of homozygous mutant mothers 
and exhibit no significant embryonic lethality.  mes-2(bn11) adult 
sterile progeny and mes-3(bn21ts) adult sterile progeny raised at the 
non-permissive temperature lack a germ line (assayed by DAPI staining).
mes-4(bn23) adult sterile progeny contain approximately 20 mitotic 
germ nuclei per gonad arm.  All sterile animals have a somatic gonad.  
Maternal effect sterility may be the null phenotype for mes-3 since 
hermaphrodites of the genotype mes-3(bn35)/sDf4, a deficiency that 
deletes the locus, produce all sterile progeny.  We feel that these 
mutations are good candidates for maternal factors required for germ 
line development because 1) lineage-specific cytoplasmic factors 
appear to be segregated normally and 2) the mutant defect is specific 
to the germ line of the progeny of mutant mothers.  mes-3 and mes-4 
map genetically to regions containing contigs and we are focussing on 
cloning these genes.

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Figure 2