Alexander kurek dissertation

The only hypothesized mechanism of recent intron gain lacking any direct evidence is that of group II intron insertion, which when demonstrated in vivo, abolishes gene expression. [35] Group II introns are therefore likely the presumed ancestors of spliceosomal introns, acting as site-specific retroelements, and are no longer responsible for intron gain. [36] [37] Tandem genomic duplication is the only proposed mechanism with supporting in vivo experimental evidence: a short intragenic tandem duplication can insert a novel intron into a protein-coding gene, leaving the corresponding peptide sequence unchanged. [38] This mechanism also has extensive indirect evidence lending support to the idea that tandem genomic duplication is a prevalent mechanism for intron gain. The testing of other proposed mechanisms in vivo, particularly intron gain during DSBR, intron transfer, and intronization, is possible, although these mechanisms must be demonstrated in vivo to solidify them as actual mechanisms of intron gain. Further genomic analyses, especially when executed at the population level, may then quantify the relative contribution of each mechanism, possibly identifying species-specific biases that may shed light on varied rates of intron gain amongst different species. [34]

Class of 1972
Debbie Cotner Augustine
Virginia Taddei Bennett
Craig Bollinger
Craig Borrell
Thomas Buttacavoli
Gerald “Jerry” James Byrnes
Thomas Cassidy
James Coutts
Dolores Grimes Downs
Patricia Louise McHugh Dugan
John Ellis
Rosemarie Eppinger
John Feather
Margaret Bowman Gallo
John Hensler
Kate Coonahan Hogan
Mary Anne Fletcher Kane
David Larkin
Philip Anthony Martinez III
James Mayer
Robert McCann, Jr.
Thomas K. Michiels
Joseph Passaretti
Francis Ragg
Donna DeJoseph Romand

Alexander kurek dissertation

alexander kurek dissertation


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