A ROLE FOR GEMIN2 IN THE REGULATION OF PREmRNA SPLICING AND CIRCADIAN RHYTHMS IN Arabidopsis

RUBÉN GUSTAVO SCHLAEN; MARCELO JAVIER YANOVSKY

San Luis

Congreso; Reunión Anual Sociedad Argentina de Investigación en Bioquímica y Biología Molecular; 2011

Sociedad Argentina de Investigación en Bioquímica y Biología Molecular

Circadian rhythms allow organisms to time biological processes to the most appropriate phases of the day. Defects in PRMT5, which transfers methyl groups to arginine residues present in histones and Sm spliceosomal proteins, impair circadian rhythms in Arabidopsis. This phenotype is caused, at least in part, by a strong alteration in alternative splicing of the clock gene PRR9. In order to test if this alteration is due to the non-methylation of Sm proteins we explored the effect of mutations that could disrupt the assembly of Sm proteins in small nuclear ribonucleopreteins (snRNPs) in a similar manner. In vertebrates, assembly of spliceosomal snRNPs is mediated by the SMN complex, composed of the proteins SMN and Gemins2–8. Arabidopsis contains orthologs of SMN and Gemin2 only. Interestingly, both of them are essential in animal cells but not in Arabidopsis. Mutations in SMN and GEMIN2 caused several developmental defects, including alteration of leaf shape, short petioles and early flowering. In addition, the gemin2 mutants displayed altered photomorphogenic responses and circadian rhythms. Moreover, genome-wide studies show that SMN and Gemin2 contribute to the regulation of a subset of pre-messenger-RNA splicing events. The circadian phenotype of gemin2 mutants is consistent with observed changes in alternative splicing of the clock gene TOC1.