New BEL-like LTR-retrotransposons in Fugu rubripes , Caenorhabditis elegans , and Drosophila melanogaster

In Caenorhabditis elegans, five proteins are required for centriole duplication: SPD-2, ZYG-1, SAS-5, SAS-6, and SAS-4. Functional orthologues of all but SAS-5 have been found in other species. In Drosophila melanogaster and humans, Sak/Plk4, DSas-6/hSas-6, and DSas-4/CPAP—orthologues of ZYG-1, SAS-6, and SAS-4, respectively—are required for centriole duplication. Strikingly, all three fly proteins can induce the de novo formation of centriole-like structures when overexpressed in unfertilized eggs. Here, we find that of eight candidate duplication factors identified in cultured fly cells, only two, Ana2 and Asterless (Asl), share this ability. Asl is now known to be essential for centriole duplication in flies, but no equivalent protein has been found in worms. We show that Ana2 is the likely functional orthologue of SAS-5 and that it is also related to the vertebrate STIL/SIL protein family that has been linked to microcephaly in humans. We propose that members of the SAS-5/Ana2/STIL family of proteins are key conserved components of the centriole duplication machinery.

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Identification of the Telomere elongation mutation in Drosophila

10.7287/peerj.preprints.26708 ◽

2018 ◽

Author(s):

Hemakumar M. Reddy ◽

Thomas A. Randall ◽

Radmila Capkova Frydrychova ◽

James M. Mason

Keyword(s):

Drosophila Melanogaster ◽

Next Generation Sequencing ◽

Ltr Retrotransposons ◽

Wild Type ◽

Dominant Mutation ◽

Site Specific ◽

Site Specific Recombination ◽

Telomere Elongation ◽

Drosophila Genetic Reference Panel ◽

Generation Sequencing

Background. Telomeres in Drosophila melanogaster are similar to those of other eukaryotes in terms of their function, although they are formed by non-LTR retrotransposons instead of telomerase-based short repeats. The length of the telomeres in Drosophila depends on the number of copies of these transposable elements. A dominant mutation, Tel1, causes a several-fold elongation of telomeres. Methods. In this study we identified the Tel1 mutation by a combination of transposon-induced, site-specific recombination and next generation sequencing. Results. Recombination located Tel1 to a 15 kb region in 92A. Comparison of the DNA sequence in this region with the Drosophila Genetic Reference Panel of wild type genomic sequences delimited Tel1 to a 3 bp deletion inside intron 8 of Ino80. Discussion. The mapped Tel1 mutation (3-bp deletion found in Ino80) did not appear to affect the quantity or length of the Ino80 transcript. Tel1 causes a significant reduction in transcripts of CG18493, a gene nested in an intron 8 of Ino80, which is expressed in ovaries and expected to encode a serine-type peptidase.

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A Genetically Marked I Element in Drosophila melanogaster Can Be Mobilized When ORF2 Is Provided in trans

Genetics ◽

10.1093/genetics/148.1.267 ◽

1998 ◽

Vol 148 (1) ◽

pp. 267-275

Author(s):

Isabelle Busseau ◽

Sophie Malinsky ◽

Maria Balakireva ◽

Marie-Christine Chaboissier ◽

Danielle Teninges ◽

...

Keyword(s):

Drosophila Melanogaster ◽

Heat Shock ◽

Reverse Transcriptase ◽

Germ Line ◽

Ltr Retrotransposons ◽

Low Frequencies ◽

High Frequencies ◽

In Trans ◽

Very High Frequencies ◽

Very High

Abstract I factors in Drosophila melanogaster are non-LTR retrotransposons similar to mammalian LINEs. They transpose at very high frequencies in the germ line of SF females resulting from crosses between reactive females, devoid of active I factors, and inducer males, containing active I factors. The vermilion marked IviP2 element was designed to allow easy phenotypical screening for retrotransposition events. It is deleted in ORF2 and therefore cannot produce reverse transcriptase. IviP2 can be mobilized at very low frequencies by actively transposing I factors in the germ line of SF females. This paper shows that IviP2 can be mobilized more efficiently in the germ line of strongly reactive females in the absence of active I factors, when it is trans-complemented by the product of ORF2 synthesized from the hsp70 heat-shock promoter. This represents a promising step toward the use of marked I elements to study retrotransposition and as tools for mutagenesis.

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