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Interstrain crosses enhance excision of Tc1 transposable elements in Caenorhabditis elegans (1990)

Mori, Ikue ; Moerman, Donald G. ; Waterston, Robert H.

Springer

Molecular genetics and genomics 220 (1990), S. 251-255

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ISSN: 1617-4623

Keywords: Caenorhabditis elegans ; Tc1 ; Mutator ; unc-22 ; Hybrid dysgenesis

Source: Springer Online Journal Archives 1860-2000

Topics: Biology

Notes: Summary We report here an unusual activation of the Tc1 transposable element system in Caenorhabditis elegans. Germline Tc1 activity, as measured by reversion of unc-22::Tc1 alleles, is elevated 50- to 100-fold by certain crosses. For example, unc-22::Tc1 reversion is 1 × 10−3 in a mut-6 IV strain and less than 1 × 10−6 in a non-mutator strain, but in the unc-22::Tc1 progeny of a cross between mut-6 hermaphrodites and non-mutator males, reversion is 10−1. The reciprocal cross does not induce this enhancement of reversion. Results similar to those for mut-6 were obtained using a mut-5 II strain. The imitator hermaphrodite by non-imitator male cross per se is not required for the enhancement of reversion, as mut-5 hermaphrodites × mut-6/+ males also induce unc-22 revertants at an elevated frequency. This reversion enhancement appears to depend on a maternal component inherited from a mutator strain, suggesting that the regulation of Tc1 activity may be complex.

Type of Medium: Electronic Resource

URL: http://dx.doi.org/10.1007/BF00260490

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Cloning, sequencing, and mapping of an α-actinin gene from the nematode Caenorhabditis elegans (1991)

Barstead, Robert J. ; Kleiman, Lawrence ; Waterston, Robert H.

New York, NY : Wiley-Blackwell

Cell Motility and the Cytoskeleton 20 (1991), S. 69-78

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ISSN: 0886-1544

Keywords: actin-membrane attachments ; cytoskeleton ; α-actinin sequence ; muscle ; Life and Medical Sciences ; Cell & Developmental Biology

Source: Wiley InterScience Backfile Collection 1832-2000

Topics: Biology , Medicine

Notes: The dense-bodies in the body wall muscle of the nematode Caenorhabditis elegans function to anchor the actin thin filaments to the adjacent sarcolemma. One of the major components of the dense-bodies is the actin-binding protein α-actinin. To facilitate a genetic analysis of α-actinin, we have cloned a cDNA encoding the nematode protein, identified its position on the nematode physical map, and developed a unique PCR based approach to test the position of the cloned gene relative to known genetic deletions. The peptide sequence deduced from the cDNA shows that, apart from a few exceptional regions, the nematode protein shows strong similarity to other known α-actinins. Its position on the genetic map shows that none of the known muscle affecting mutations identified in C. elegans are in this α-actinin gene. This gene has been given the name atn-1 (α-actinin-1).

Additional Material: 7 Ill.