INTRON42

Evolution of eukaryotic intron splicing

Coordinatore	MAGYAR TUDOMANYOS AKADEMIA SZEGEDI BIOLOGIAI KOZPONTJA    more  Organization address address: Temesvari krt. 62 city: SZEGED postcode: 6701 contact info Titolo: Dr. Nome: Miklós Cognome: Erdélyi Email: send email Telefono: +36 62 599686 Fax: +36 62 433503
Nazionalità Coordinatore	Hungary [HU]
Totale costo	190˙113 €
EC contributo	190˙113 €
Programma	FP7-PEOPLE Specific programme "People" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013)
Code Call	FP7-PEOPLE-2013-IIF
Funding Scheme	MC-IIF
Anno di inizio	2014
Periodo (anno-mese-giorno)	2014-07-01   -   2016-06-30

 Partecipanti

#	participant	country	role	EC contrib. [€]
1	MAGYAR TUDOMANYOS AKADEMIA SZEGEDI BIOLOGIAI KOZPONTJA  Organization address address: Temesvari krt. 62 city: SZEGED postcode: 6701 contact info Titolo: Dr. Nome: Miklós Cognome: Erdélyi Email: send email Telefono: +36 62 599686 Fax: +36 62 433503	HU (SZEGED)	coordinator	190˙113.60

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 Obiettivo del progetto (Objective)

'Introns are non-coding intervals that interrupt the coding sequences of eukaryotic genes. Intron removal is performed by a complicated molecular machinery, called the spliceosome, concomitantly with gene transcription. Introns and the splicing machinery (or at least their traces) are found in every sequenced eukaryotic genome. Moreover, many introns are found at homologous positions across different kingdoms, suggesting that some originate in the earliest eukaryotes.

Introns are largely devoid of function, yet in humans (and mammals in general), they make up more than~40% of the genome. The most obvious evolutionary advantage of the interrupted coding sequences is that they increase functional complexity by enabling alternate assemblies. Introns provide a powerful source of variations for natural selection in many other ways, since splicing is tightly coupled with transcription and export from the nucleus, and intronic sequences frequently harbor regulatory elements.

The proposed project aims at developing bioinformatics tools and mathematical models that help understanding randomness and natural selection that shape exon-intron architecture in different eukaryotic lineages. In particular, we will investigate intron turnover in fast-evolving genes, selective constraints on intron length and mechanisms of intron gain on a large scale, using annotated whole genomes. In addition to providing new insights into the ways evolution affects gene structure, the developed methods will be useful to produce better annotations of coding regions and functional intronic elements.'