Multiple mechanisms modulate cap -dependent translation during mitosis
A majority of cellular mRNAs is translationally silent during the M-phase of the cell cycle. A subset of mRNAs, however, retains the ability to undergo translation. It is thought that the presence of IRES (internal ribosome entry site) elements in these cellular mRNAs enables them to be translationally competent during mitosis. The precise mechanism by the switch from canonical cap-dependent translation to the IRES mode during G2/M occurs is not well understood. Some of the molecular interactions involved in downregulation of translation during mitosis have been described in this work. Biochemical studies show that there are no changes either in levels or in composition of the eukaryotic initiation factor complex proteins. A majority of mRNAs remains associated with the initiation complex and several mRNAs are maintained on polysomes. Microarray analyses show that the transcripts that show an increased association with eIF4G do not correlate with increased translation efficiency. Interestingly, eIF4E fails to become dephosphorylated. In this work I have proposed a mechanism that encompasses these observations.
4E-BP1 and Raptor, both downstream components of the mTOR kinase pathway undergo phosphorylation modifications during mitosis. The cellular function of these modifications is not known. Biochemical studies performed address this important cellular pathway in the context of the G2/M phase of the cell cycle