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The New Biologist,
1990]
DNA rearrangements are responsible for a variety of phenomena in unicellular organisms, such as bacterial or protozoan antigenic variation, yeast mating type switching, and bacterial nitrogen fixation. In multicellular organisms, however, DNA rearrangements do not seem to be a major contributor to cell determination; in fact the only mammalian tissue in which rearrangements play an identified vital role, the immune system, could be viewed as a collection of unicellular organisms. Perhaps in multicellular organisms there are sufficient alternative strategies to determine the fate of cell lineages, and the costs or risks of reshuffling the genome may be too high. Nevertheless, transposons are probably found in all organisms. Why?
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Methods Cell Biol,
1995]
Genetic balancers are genetic constructs or chromosomal rearrangements that allow lethal or sterile mutations to be stably maintained in heterozygotes. In this chapter we use the term balancer primarily to refer to chromosomal duplications or rearrangements that suppress crossing over. In addition, we define lethal as any mutation that blocks survival or reproduction. Phenotypes associated with lethal mutations in Caenorhabditis elegans range from egg or larval lethality to adult sterility and maternal effect lethality, and can include conditional effects such as temperature sensitivity. The number of essential genes in C. elegans (those identified by lethal mutations) may range as high as 7000 according to genetic estimates. Thus, lethal mutations constitute a rich source of information about basic biological processes in this nematode.
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Dev Genet,
1994]
The nematode Caenorhabditis elegans has been the subject of many detailed investigations in developmental biology. Molecular analyses have failed to detect covalent alterations to DNA, such as methylation or rearrangement, during development of C. elegans. Genetic experiments indicate that imprinting of gamete genomes does not occur to any significant extent. The maintenance of gene activity states in this organism may depend predominantly on regulatory gene circuitry. Some possible examples of maintenance circuits are discussed.
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Nat Rev Mol Cell Biol,
2003]
Non-homologous DNA end-joining (NHEJ)--the main pathway for repairing double-stranded DNA breaks--functions throughout the cell cycle to repair such lesions. Defects in NHEJ result in marked sensitivity to ionizing radiation and ablation of lymphocytes, which rely on NHEJ to complete the rearrangement of antigen-receptor genes. NHEJ is typically imprecise, a characteristic that is useful for immune diversification in lymphocytes, but which might also contribute to some of the genetic changes that underlie cancer and ageing.
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J Cell Sci,
2002]
Asymmetric cell division can produce daughter cells with different developmental fates and is often accompanied by a difference in cell size. A number of recent genetic and in vivo imaging studies in Drosophila and Caenorhabditis elegans have begun to elucidate the mechanisms underlying the rearrangements of the cytoskeleton that result in eccentrically positioned cleavage planes. As a result, we are starting to gain an insight into the complex nature of the signals controlling cytoskeletal dynamics in the dividing cell. In this commentary we discuss recent findings on how the mitotic spindle is positioned and on cleavage site induction and place them in the context of cell size asymmetry in different model organisms.
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Curr Opin Genet Dev,
2021]
Homologous recombination (HR) plays a critical role in largely error-free repair of mitotic and meiotic DNA double-strand breaks (DSBs). DSBs are one of the most deleterious DNA lesions, which are repaired by non-homologous end joining (NHEJ), homologous recombination (HR) or, if compromised, micro-homology mediated end joining (MMEJ). If left unrepaired, DSBs can lead to cell death or if repaired incorrectly can result in chromosome rearrangements that drive cancer development. Here, we describe recent advances in the field of mitotic HR made using Caenorhabditis elegans roundworm, as a model system.
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Trends in Cell Biology,
1996]
Cellular microtubules assemble and disassemble at a variety of rates and frequencies, and these properties contribute directly to the cell-cycle-associated rearrangements of the microtubule cytoskeleton and to the molecular basis of mitosis. The kinetics of assembly/disassembly are governed, in part, by the hydrolysis of GTP bound to the B-tubulin nucleotide-binding site. The B-tubulin GTP-binding site, therefore, lies at the heart of microtubule assembly-disassembly kinetics, and the elucidation of its structure is central to an understanding of the cellular behaviour of microtubules. Unfortunately, the crystallographic structure of B-tubulin is not yet available. In this review, we describe the progress being made using mutagenesis and biochemical studies to understand the structure of this unusual GTP-binding site.
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Results Probl Cell Differ,
2011]
Throughout the development of an organism, it is essential that the cell cycle machinery is fine-tuned to generate cells of different fate. A series of asymmetric cell divisions leads to lineage specification. The Caenorhabditis elegans embryo is an excellent system to study various aspects of the early embryonic cell cycle. The invariant nature of the rapid cell divisions is the key feature for studying the effects of small perturbations to a complex process such as the cell cycle. The thorough characterization of the asymmetric first cell division of the C. elegans embryo has given great insight on how the oscillations of the cell cycle coordinate with the cytoplasmic rearrangements that ultimately lead to two developmentally distinct daughter cells.
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Trends Genet,
2013]
Thirty years after the identification of WNTs, understanding of their signal transduction pathways continues to expand. Here, we review recent advances in characterizing the Wnt-dependent signaling pathways in Caenorhabditis elegans linking polar signals to rearrangements of the cytoskeleton in different developmental processes, such as proper mitotic spindle orientation, cell migration, and engulfment of apoptotic corpses. In addition to the well-described transcriptional outputs of the canonical and noncanonical Wnt pathways, new branches regulating nontranscriptional outputs that control RAC (Ras related GTPase) activity are also discussed. These findings suggest that Wnt signaling is a master regulator not only of development, but also of cell polarization.
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Development,
2007]
The symmetry-breaking event during polarization of C. elegans embryos is an asymmetric rearrangement of the acto-myosin network, which dictates cell polarity through the differential recruitment of PAR proteins. The sperm-supplied centrosomes are required to initiate this cortical reorganization. Several questions about this event remain unanswered: how is the acto-myosin network regulated during polarization and how does acto-myosin reorganization lead to asymmetric PAR protein distribution? As we discuss, recent studies show that C. elegans embryos use two GTPases, RHO-1 and CDC-42, to regulate these two steps in polarity establishment. Although RHO-1 and CDC-42 control distinct aspects of polarization, they function interdependently to regulate polarity establishment in C. elegans embryos.