Abstract
Spatial separation of eukaryotic cells into the nuclear and cytoplasmic compartment permits uncoupling of DNA transcription from translation of mRNAs and allows cells to modify newly transcribed pre mRNAs extensively. Intronic sequences (introns), which interrupt the coding elements (exons), are excised ("spliced") from pre-mRNAs in the nucleus to yield mature mRNAs. This not only enables alternative splicing as an important source of proteome diversity, but splicing is also an essential process in all eukaryotes and knock-out or knock-down of splicing factors frequently results in defective cell proliferation and cell division. However, higher eukaryotes progress through cell division only after breakdown of the nucleus ("open mitosis"). Open mitosis suppresses basic nuclear functions such as transcription and splicing, but allows separate, mitotic functions of nuclear proteins in cell division. Mitotic defects arising after loss-of-function of splicing proteins therefore could be an indirect consequence of compromised splicing in the closed nucleus of the preceding interphase or reflect a direct contribution of splicing proteins to open mitosis. Although experiments to directly distinguish between these two alternatives have not been reported, indirect evidence exists for either hypotheses. In this review, we survey published data supporting an indirect function of splicing in open mitosis or arguing for a direct function of spliceosomal proteins in cell division.