Evidence for a transposon in caenorhabditis elegans

Emmons, Scott W.; Yesner, Lewis; Ruan, Ke san; Katzenberg, D R

doi:10.1016/0092-8674(83)90496-8

Cited by 247 publications

(184 citation statements)

References 27 publications

Supporting

Mentioning

174

Contrasting

Unclassified

Order By: Relevance

“…pALl and pAL5 each contain one of the collagen genes from cosmid ZK857. The pAL5 probe revealed a 1.6-kb band shift in strains DR1048 and JK1012, the size expected for insertion of the C. elegans transposon Tcl (Emmons et al, 1983). DNA from revertant strain DR1049 showed the wildtype band size.…”

Section: Resultsmentioning

confidence: 99%

Molecular and genetic analyses of the Caenorhabditis elegans dpy-2 and dpy-10 collagen genes: a variety of molecular alterations affect organismal morphology.

Levy

Yang

Kramer

1993

MBoC

View full text Add to dashboard Cite

We have identified and cloned the Caenorhabditis elegans dpy-2 and dpy-10 genes and determined that they encode collagens. Genetic data suggested that these genes are important in morphogenesis and possibly other developmental events. These data include the morphologic phenotypes exhibited by mutants, unusual genetic interactions with the sqt-1 collagen gene, and suppression of mutations in the glp-1 and mup-i genes. The proximity of the dpy-2 and dpy-10 genes (3.5 kilobase) and the structural similarity of their encoded proteins (41% amino acid identity) indicate that dpy-2 and dpy-10 are the result of a gene duplication event. The genes do not, however, appear to be functionally redundant, because a dpy-10 null mutant is not rescued by the dpy-2 gene. In addition, full complementation between dpy-2 and dpy-10 can be demonstrated with all recessive alleles tested in trans. Sequence analysis of several mutant alleles of each gene was performed to determine the nature of the molecular defects that can cause the morphologic phenotypes. Glycine substitutions within the Gly-X-Y portion of the collagens can result in dumpy (Dpy), dumpy, left roller (DLRol), or temperature-sensitive DLRol phenotypes. dpy-1O(cn64), a dominant temperature-sensitive DLRol allele, creates an Arg-to-Cys substitution in the amino non-Gly-X-Y portion of the protein. Three dpy-10 alleles contain Tcl insertions in the coding region of the gene. dpy-lO(cg36) (DLRol) creates a nonsense codon near the end of the Gly-X-Y region. The nature of this mutation, combined with genetic data, indicates that DLRol is the null phenotype of dpy-10. The Dpy phenotype results from reduced function of the dpy-1O collagen gene. Our results indicate that a variety of molecular defects in these collagens can result in severe morphologic changes in C. elegans.

show abstract

Section: Resultsmentioning

confidence: 99%

Molecular and genetic analyses of the Caenorhabditis elegans dpy-2 and dpy-10 collagen genes: a variety of molecular alterations affect organismal morphology.

Levy

Yang

Kramer

1993

MBoC

View full text Add to dashboard Cite

show abstract

“…The mariner and Tc1 elements were found in D. mauritiana (Jacobson et al, 1986) and the nematode Caenorhabditis elegans (Emmons et al, 1983), respectively, and related elements are known to occur in diverse taxa, including planarians (Garcia-Fernandez et al, 1995), annelids (Jee et al, 2007), vertebrates (Smit and Riggs, 1996), plants (Jarvik and Lark, 1998) and fungi (Langin et al, 1995). Manifestation of such a wide distribution leads to the inference that elements of this family require no or few factors produced from host cells for their transposition reaction.…”

Section: Introductionmentioning

confidence: 99%

The Tol1 element of the medaka fish, a member of the hAT transposable element family, jumps in Caenorhabditis elegans

Takagi

Koga

2008

Heredity

View full text Add to dashboard Cite

Tol1 is a DNA-based transposable element residing in the genome of the medaka fish Oryzias latipes, and has been proven to be transposed in various vertebrate species, including mammals. This element belongs to the hAT (hobo/ Activator/Tam3) transposable element family, whose members are distributed in a wide range of organisms. It is thus possible that Tol1 is mobile in organisms other than vertebrates. We here show that transposition of this element occurs in the nematode Caenorhabditis elegans. A donor plasmid containing a Tol1 element and a helper plasmid carrying the transposase gene were delivered into gonad cells and, after several generations of culturing, were recovered from worms. PCR analysis of the donor plasmid, using primers that encompassed the Tol1 element, revealed excision of the Tol1 portion from the plasmid. Analysis of genomic DNA of the worms by the inverse PCR method provided evidence that Tol1 had been integrated into the C. elegans chromosomes. Vertebrates and C. elegans are phylogenetically distantly related organisms in that the former are deuterostomes and the latter a protostome animal. Our results indicate (1) the transposition reaction of the Tol1 element requires, besides the transposase, no factors from host cells, or (2) the host factors, even if required, are those that are common to protostomes and deuterostomes. The results also have significance for the development of a gene transfer vector and other biotechnology tools for C. elegans.

show abstract

“…This suggested the existence of a mechanism that prevents DNA transposition, thus protecting the succeeding generation from the associated detrimental effects. Indeed, mutants that have lost this silencing can be isolated (and even a natural variant exist: the Bergerac BO strain), and as a consequence of active transposition, these strains display increased levels of 'spontaneous' mutations, hence these mutant alleles have been named mut to indicate their mutator phenotype (Emmons et al, 1983;Collins et al, 1987). As a result of high levels of genome instability such strains become sick and eventually die when maintained as individual clones, which illustrates the importance of taming the activity of such molecular parasites.…”

Section: Mutator Phenotypes In C Elegansmentioning

confidence: 99%

Genomic instability and cancer: scanning the Caenorhabditis elegans genome for tumor suppressors

2004

View full text Add to dashboard Cite

Maintaining the stability of the genome is critical to normal cell growth and development. The early notion that cancer is the result of mutations in genes controlling cellular growth implied that gene or genome integrity is vital to the prevention of oncogenesis, and many genes and pathways that prevent genomic deterioration have been identified over the past decades. Recent progress in reverse genetic approaches, principally RNA interference, now allows the systematic analysis of gene function on a genomic scale in an animal system. Here, we discuss genomic approaches in the model organism Caenorhabditis elegans, aimed to identify genes and genetic networks that contribute to genome stability and are thus potentially involved in human carcinogenesis.

show abstract

Evidence for a transposon in caenorhabditis elegans

Cited by 247 publications

References 27 publications

Molecular and genetic analyses of the Caenorhabditis elegans dpy-2 and dpy-10 collagen genes: a variety of molecular alterations affect organismal morphology.

Molecular and genetic analyses of the Caenorhabditis elegans dpy-2 and dpy-10 collagen genes: a variety of molecular alterations affect organismal morphology.

The Tol1 element of the medaka fish, a member of the hAT transposable element family, jumps in Caenorhabditis elegans

Genomic instability and cancer: scanning the Caenorhabditis elegans genome for tumor suppressors

Contact Info

Product

Resources

About