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Riddle DL, Blumenthal T, Meyer BJ, et al., editors. C. elegans II. 2nd edition. Cold Spring Harbor (NY): Cold Spring Harbor Laboratory Press; 1997.

Cover of C. elegans II

C. elegans II. 2nd edition.

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Section IITc1 and Tc3

Molecular and genetic approaches led to the discovery of the first transposable element in C. elegans: Tc1 (an amusing account of its discovery was published by Anderson et al. [1992]). Emmons and Hirsh noticed the frequent polymorphism between genomic clones of different strains (Emmons et al. 1979), one of which proved to be caused by a Tc1 insertion (Emmons et al. 1983). Rozenzweig et al. (1983a) and Liao et al. (1983) discovered a Tc1 element while cloning and sequencing actin genes. These molecular approaches identified Tc1 elements, but it took genetic approaches to establish the mobile nature of Tc1. Eide and Anderson (1985b), 1988 used the unc-54 myosin gene as a target to trap transposons, and Moerman and Waterston (1984) and Moerman et al. (1986) made use of the mobile nature of Tc1 to clone another muscle gene, unc-22 , by transposon tagging.

Tc1 is an element of 1610 bp with 54-bp terminal inverted repeats (Fig. 1) (Rosenzweig et al. 1983a). Tc1 elements always integrate into the sequence TA (Rosenzweig et al. 1983a; Eide and Anderson 1988; Mori et al. 1988b; Zwaal et al. 1993; van Luenen and Plasterk 1994). The copy number of Tc1 is strain-dependent: The Bristol N2 strain contains approximately 30 copies of Tc1, whereas the Bergerac BO strain contains more than 500 Tc1 copies per haploid genome (Emmons et al. 1983; Liao et al. 1983; Egilmez et al. 1995).

Figure 1. Structure of the DNA transposons of C.

Figure 1

Structure of the DNA transposons of C. elegans. (Black boxes) Inverted repeats; (arrows) open reading frames.

The Tc1 insertion pattern within the C. elegans species shows interesting features. The copies present in the standard laboratory strain Bristol N2 (the genome of which is being sequenced) are also present in high-copy-number strains (Egilmez et al. 1995). In addition, high-copy-number strains such as Bergerac contain at least 500 additional Tc1 insertions. Comparison of a limited number of Tc1 insertion sites among different high-copy-number strains shows that these strains often contain a subset of the Bergerac elements, such that regions of the genome either are completely devoid of the Bergerac Tc1 copies or contain the entire set (Egilmez et al. 1995). This patchy distribution suggests that these strains arose by crosses of a high-copy-number strain with a low-copy-number strain.

The Tc1 element contains one large open reading frame that was initially thought to encode a 273-amino-acid Tc1 transposase (Rosenzweig et al. 1983a). This protein was produced in Escherichia coli and was found to have a strong but nonspecific affinity for DNA (Schukkink and Plasterk 1990). However, transposition requires a specific interaction of the transposase with the transposon DNA. Sequence comparisons with other Caenorhabditis species (Schukkink and Plasterk 1990; Prasad et al. 1991) and cDNA analysis (Vos et al. 1993) indicated the presence of a small 5′exon and suggested that the complete coding region might be 343 triplets long. Expression of this larger protein (Tc1A) in the Bristol N2 strain results in enhanced somatic transposition of Tc1 (Vos et al. 1993). Furthermore, Tc1A purified to 95% homogeneity from a recombinant E. coli strain was recently shown to be sufficient for mediating Tc1 excision and transposition in vitro (Vos et al. 1996). The Tc1A-specific DNA-binding domain is largely contained within the extra 5′exon, explaining the lack of specific binding by the 273-amino-acid protein. The properties of 343-amino-acid Tc1 transposase (Tc1A) are discussed below.

The Tc3 element is present in approximately 15 copies per haploid genome in all strains analyzed thus far (Collins et al. 1989). Tc3 is 2335 bp long and has terminal inverted repeats of 462 bp (Fig. 1). The element contains a gene composed of two exons encoding Tc3A, the 327-amino-acid transposase of Tc3 (van Luenen et al. 1993). This conclusion is based on arguments similar to those for Tc1A. Forced expression of Tc3A induces Tc3 transposition in vivo, and recombinant Tc3A binds specifically to the Tc3 inverted repeats in vitro.

Tc1 and Tc3 have several common characteristics (Collins et al. 1989). The proteins encoded by the two elements are 34% identical. The terminal nine nucleotides of Tc1 and Tc3 are almost identical. Both elements integrate exclusively into the sequence TA, and transposition activity of both elements is affected by the same “host” mutation (the mut-2 mutation discussed below).

Copyright © 1997, Cold Spring Harbor Laboratory Press.
Bookshelf ID: NBK20113
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