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The availability of complete genome sequences has revealed that genomes contain numerous mobile genetic elements. The activity of these transposons results in genome instability. In the nematode Caenorhabditis elegans, transposition is silenced in the germline, protecting the genome from heritable defects that are caused by transposon jumps. The discovery of RNA interference (RNAi) has greatly increased our understanding of this genome-defense mechanism because transposon silencing and RNAi share common factors. RNAi is the post-transcriptional silencing of a gene in response to double-stranded RNA (dsRNA), which is processed into small interfering RNAs (siRNAs) that mediate sequence-specific RNA degradation. Indeed, transposon-derived dsRNA and siRNAs are detected in vivo and are capable of inducing silencing. In addition, many new genes have been identified that are required for the silencing of transposons. In this article, we discuss our current model for transposon silencing and address several unanswered questions because many aspects of this protection mechanism in C. elegans might be present in a broad range of organisms. [Copyright &y& Elsevier]

Genomes are databases sensitive to invasion by viruses. In recent years, a defense mechanism has been discovered, which turns out to be conserved among eukaryotes. The system can be compared to the immune system in several ways: It has specificity against foreign elements and the ability to amplify and raise a massive response against an invading nucleic acid. The latter property is beginning to be understood at the molecular Level. [ABSTRACT FROM AUTHOR]

Identifies Caenorhabditis elegans (C. elegans) as the first animal genome to be sequenced. Determination of the complete pattern of cell divisions which creates the somatic cells in the adult animal; Dependency of classical genetics on the isolation of mutants with clearly defined phenotypes; Possibility of transiently and genetically mutating genes in C. elegans.

Single nucleotide polymorphisms (SNPs) are the most common genetic variation in mammalian populations. Their significance is illustrated by their potential contribution to common disease but also by their potential for use in genetic association and mapping experiments. We have examined the genetic variation between commonly used inbred rat strains by using an efficient SNP discovery and typing assay based on enzyme-based (CEL I) heteroduplex cleavage. Screening of a panel of 96 different rat (sub-)strains for 100 genomic loci in 55 genes, whose human homologs are implicated in clinically relevant diseases like neurological disorder, cancer, schizophrenia, and obesity, resulted in the identification of 103 novel polymorphisms. As all strains are simultaneously genotyped in this setup, this allowed us to make an estimate of the genetic variation between and within commonly used rat inbred strains. Interestingly, we observed substantial genetic variation between colonies of the same inbred strain, maintained at different locations. Furthermore, we identified 17 non-synonymous SNPs that may have an effect on protein function and contribute to phenotypic differences between different laboratory strains. [ABSTRACT FROM AUTHOR]

The rat is one of the most extensively studied model organisms, and with its genome being sequenced, tools to manipulate gene function in vivo have become increasingly important. We here report proof of principle for target-selected mutagenesis as a reverse genetic or knockout approach for the rat. [Copyright &y& Elsevier]

Transposon jumps are a major cause of genome instability. In the C. elegans strain Bristol N2, transposons are active in somatic cells, but they are silenced in the germline , presumably to protect the germline from mutations. Interestingly, the transposon-silencing mechanism shares factors with the RNAi machinery . To better understand the mechanism of transposon silencing, we performed a genome-wide RNAi screen for genes that, when silenced, cause transposition of Tc1 in the C. elegans germline. We identified 27 such genes, among which are mut-16, a mutator that was previously found but not identified at the molecular level, ppw-2, a member of the argonaute family, and several factors that indicate a role for chromatin structure in the regulation of transposition. Some of the newly identified genes are also required for cosuppression and therefore represent the shared components of the two pathways. Since most of the newly identified genes have clear homologs in other species, and since transposons are found from protozoa to human, it seems likely that they also protect other genomes against transposon activity in the germline. [Copyright &y& Elsevier]

Presents a study that identified genes that protect the Caenorhabditis elegans genome against mutations by genome-wide RNAi. Method of the study; Results and discussion; Conclusion.