Effects of chromosomal deficiencies on early cleavage patterning and terminal phenotype in Caenorhabditis elegans embryos

Abstract

We have analyzed pregastrulation cleavage patterns in Caenorhabditis elegans embryos homozygous for various chromosomal deficiencies. By two different estimates these deficiencies represent between 37 and 49% of the genome, including the entire X chromosome and substantial portions of each of the five autosomes. Among these genomic regions, we find none whose absence causes defects in pregastrulation cleavage patterns. We can conclude that there are at most very few genes whose transcription after fertilization is required for normal early patterning of cell divisions. We also scored terminal phenotypes of the homozygous deficiency embryos for stage of arrest and for expression of three tissue-specific differentiation markers. Based on these phenotypes, we have identified regions of the genome that are required for completion of cell proliferation, expression of gut differentiation and entry into morphogenesis. Somewhat surprisingly, embryos in which cell proliferation is arrested at less than 20% of the normal cell number can nevertheless initiate morphogenesis and undergo elongation to the twofold stage. Our results are consistent with the view that many early events in C. elegans embryogenesis are controlled exclusively by maternally produced gene products. However, they are also consistent with the likely possibility that, at least in some deficiency embryos, although cleavage patterns may be normal, blastomere identities are not. In this respect the early cleavages may differ from later lineages, in which cell division patterns appear to be characteristic of cell identity.