Changes in subcellular structures and states of pumilio 1 regulate the translation of target Mad2 and cyclin B1 mRNAs
- Takei, N., Takada, Y., Kawamura, S., Sato, K., Saitoh, A., Bormann, J., Yuen, W.S., Carroll, J., Kotani, T.
- Journal of Cell Science 133(23): (Journal)
- Registered Authors
- Kotani, Tomoya
- Meiosis, Oocyte, Pumilio 1, Translational control, Vertebrate, mRNA localization
- MeSH Terms
- Cyclin B1*/genetics
- Cyclin B1*/metabolism
- Mad2 Proteins/genetics*
- Protein Biosynthesis*
- RNA, Messenger/genetics
- RNA, Messenger/metabolism
- RNA-Binding Proteins/chemistry*
- 33148609 Full text @ J. Cell Sci.
Takei, N., Takada, Y., Kawamura, S., Sato, K., Saitoh, A., Bormann, J., Yuen, W.S., Carroll, J., Kotani, T. (2020) Changes in subcellular structures and states of pumilio 1 regulate the translation of target Mad2 and cyclin B1 mRNAs. Journal of Cell Science. 133(23):.
Temporal and spatial control of mRNA translation has emerged as a major mechanism for promoting diverse biological processes. However, the molecular nature of temporal and spatial control of translation remains unclear. In oocytes, many mRNAs are deposited as a translationally repressed form and are translated at appropriate times to promote the progression of meiosis and development. Here, we show that changes in subcellular structures and states of the RNA-binding protein pumilio 1 (Pum1) regulate the translation of target mRNAs and progression of oocyte maturation. Pum1 was shown to bind to Mad2 (also known as Mad2l1) and cyclin B1 mRNAs, assemble highly clustered aggregates, and surround Mad2 and cyclin B1 RNA granules in mouse oocytes. These Pum1 aggregates were dissolved prior to the translational activation of target mRNAs, possibly through phosphorylation. Stabilization of Pum1 aggregates prevented the translational activation of target mRNAs and progression of oocyte maturation. Together, our results provide an aggregation-dissolution model for the temporal and spatial control of translation.
Genes / Markers
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Engineered Foreign Genes