In C. elegans, the embryonic germ line is defined during the first four rounds of division. In contrast to the soma, the germ line cells (P-cells) divide asymmetrically in a stem-cell-like manner. To understand the mechanisms underlying this asymmetry, we analysed maternal lethal mutants in three genes with major defects in the embryonic germ line. In
cib-1 (changed identity of blastomeres, Schnabel and Schnabel, 1990),
cib-2 and
cib-3 the germ line cells P1 to P3 divide symmetrically instead of asymmetrically after a delay of up to one cell cycle. In
cib-2, after a prolonged cytokinesis during the first mitosis, no nuclei are formed in the 2-cell-stage. This first defect results from failed chromosome condensation and causes DNA fragmentation during cell division. As a consequence, the cell cycle control
atl-1 chk-1 (Brauchle et al., 2003) is activated. We confirmed, that the activation of the cell cycle control depends on the damaged DNA by laser irradiation of one pronucleus in the wild-type embryo, which phenocopies the
cib-2 mutant. Since
cib-1 codes for the only homologe of a thymidylate synthase (Winska et al., 2005) in worms, we assume the P-cell phenotype caused by mutations in
cib-1 and
cib-2 are due to a reduced DNA integrity. To our surprise the phenotype is germ line specific, which suggests the existence of a germ line specific DNA integrity checkpoint. CIB-3, in contrast, is essential for the organisation of the asymmetric cytoplasmic distribution of germ line specific factors. Nevertheless, CIB-2 and CIB-3 have identical interaction proteins in a Yeast-Two-Hybrid screen. This indicates a linkage between DNA integrity and the organisation of cytoplasmic polarity. Thus, the system may serve to survey integrity of the worm population, by eliminating embryos with defect germ line DNA.