Maternal-effect lethal mutations on linkage group II of Caenorhabditis elegans.

Abstract

We have analyzed a set of linkage group (LG) II maternal-effect lethal mutations in Caenorhabditis elegans isolated by a new screening procedure. Screens of 12,455 F1 progeny from mutagenized adults resulted in the recovery of 54 maternal-effect lethal mutations identifying 29 genes. Of the 54 mutations, 39 are strict maternal-effect mutations defining 17 genes. These 17 genes fall into two classes distinguished by frequency of mutation to strict maternal-effect lethality. The smaller class, comprised of four genes, mutated to strict maternal-effect lethality at a frequency close to 5 X 10(-4), a rate typical of essential genes in C. elegans. Two of these genes are expressed during oogenesis and required exclusively for embryogenesis (pure maternal genes), one appears to be required specifically for meiosis, and the fourth has a more complex pattern of expression. The other 13 genes were represented by only one or two strict maternal alleles each. Two of these are identical genes previously identified by nonmaternal embryonic lethal mutations. We interpret our results to mean that although many C. elegans genes can mutate to strict maternal-effect lethality, most genes mutate to that phenotype rarely. Pure maternal genes, however, are among a smaller class of genes that mutate to maternal-effect lethality at typical rates. If our interpretation is correct, we are near saturation for pure maternal genes in the region of LG II balanced by mnC1. We conclude that the number of pure maternal genes in C. elegans is small, being probably not much higher than 12.

Tissue-specific regulation of epidermal contraction during Caenorhabditis elegans embryonic morphogenesis

“…Extragenic transgenes were generated for mel-11 cDNA driven by either the endogenous, pceh-16 or pelt-3 promoters and were examined for rescue of the ts allele mel-11(it26) [hereafter referred to as mel-11(ts) , Supplementary Table S4]. This mutation produces 100% unhatched embryos at 25° ( Kemphues et al 1988 ; Wissmann et al 1997 ). Three independent mel-11 cDNA lines driven by the endogenous pmel-11 promoter ( sbEx254 , sbEx255 , and sbEx256 ) rescued the 25° lethal phenotype with 63%, 31%, and 37% hatching, respectively ( P < 0.0005, Figure 3A ).…”

On the origins and conceptual frameworks of natural plasticity—Lessons from single-cell models in C. elegans

“…Early ablations of individual blastomeres and blastomere fusion experiments initially supported the view that C. elegans development was cell-intrinsically specified (Junkersdorf and Schierenberg, 1992;Schierenberg, 1984;Stevens, 1909;Sulston et al, 1983). Moreover the culture of isolated founder blastomeres suggested that they generate largely the same tissue types as they do in an intact embryo (Laufer et al, 1980;Priess and Thomson, 1987) Several years of subsequent investigations, including beautiful maternal-effect lethal forward genetic screens (Kemphues et al, 1988) However, it is now clear that early blastomeres are not only specified in a cell-intrinsic manner but require cell-signalling events to drive alternative fates and are much more plastic than originally thought. Elegant blastomere manipulation experiments and the examination of genetic mutants have provided evidence for several non-autonomous signalling interactions involving predominantly the Notch-and Wnt-signalling pathways between early blastomeres (reviewed in (Priess, 2005; Sawa and Korswagen, 2013)) .…”

The molecular underpinnings of fertility: Genetic approaches in Caenorhabditis elegans

“…Multiple groups have carried out such screens and due to space limits, their screening strategies were not discussed in detail here. 57 – 59 , 61 , 64 , 64 Sometimes sterile mutants from these screens are shared with us by the community and found to define novel fertility genes (Reference 20 and our unpublished data). Other times sterile mutants were misclassified as embryonic lethal and sometimes discarded.…”

“…To better understand sperm-oocyte interactions, the Singson lab developed a screening strategy ( Figure 3B ) based on screens that looked for maternal-effect embryonic lethal mutants. 57 – 61 The goal of this screen is to find ts mutants in which sterility results from defects in sperm-oocyte interactions. To facilitate mutant selection, we use a starter strain that carries a sem-2 mutation and an embryonic gut marker 22 ( Figure 3B ).…”