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Gewählte Publikation:

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Publikationstyp: Dissertation
Dokumenttyp:

Jahr: 2010

AutorInnen: Meduri, Eshwar

Titel: Intron Evolution in Drosophila.

Titelvariante: Intron Evolution in Drosophila

Quelle: Dissertation, Vet. Med. Univ. Wien, pp. 94.


Betreut von:

Schlötterer Christian

Begutachtet von:
Müller Mathias
Schlötterer Christian

Einrichtung:
Institut für Populationsgenetik


Abschluss Datum: 08.03.10


Abstract:
A typical eukaryotic protein coding gene contains exons which are translated to proteins intervened by non-coding parts called introns. Introns are spliced out by spliceosome before RNA leaves the nucleus, complex machinery consisting of several small nuclear ribonucleoproteins (snRNP). Introns are present in all eukaryotic species. Their average numbers per gene vary drastically between species with 8 introns/gene, 5.3 introns/gene and 2.8 introns/ gene in Homo sapiens, Caenorhabditis elegans and Drosophila melanogaster respectively (ROY and GILBERT 2006). There has been long lasting debate going on about the origin and the proliferation of introns in the eukaryotic genomes despite more than 30 years of extensive research. The paucity of intron gains and losses remains a big challenge to understand the mechanisms of intron gains and losses in eukaryotic genomes. However, the availability of genomic sequences for 12 Drosophila species (CLARK et al. 2007), and Drosophila melanogaster being a model organism, provides an excellent opportunity to study the evolution of introns in a phylogenetic framework. In this thesis intron gain and loss events were predicted along the respective branches in Drosophila clade to study the mechanisms responsible for these events and the evolutionary forces acting for the proliferation of introns.

Schlagworte:
Intron gains and losses / Evolution / Drosophila


Im Rahmen der Hochschulschrift entstandene Publikation(en):

Farlow, A; Meduri, E; Dolezal, M; Hua, L; Schlötterer, C (2010): Nonsense-mediated decay enables intron gain in Drosophila. PLoS Genet. 2010; 6(1):e1000819
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