Abstract
There are multiple isoforms of p90 ribosomal S6 kinase (RSK), which regulate diverse cellular functions such as cell growth, proliferation, maturation, and motility. However, the relationship between the structures and functions of RSK isoforms remains undetermined. Artemia is a useful model in which to study cell cycle arrest because these animals undergo prolonged diapauses, a state of obligate dormancy. A novel RSK isoform was identified in Artemia, which was termed Ar-Rsk2. This isoform was compared with an RSK isoform that we previously identified in Artemia, termed Ar-Rsk1. Ar-Rsk2 has an ERK-docking motif, whereas Ar-Rsk1 does not. Western blot analysis revealed that Ar-Rsk1 was activated by phosphorylation, which blocked meiosis in oocytes. Knockdown of Ar-Rsk1 reduced the level of phosphorylated cdc2 and thereby suppressed cytostatic factor activity. This indicates that Ar-Rsk1 regulates the cytostatic factor in meiosis. Expression of Ar-Rsk2 was down-regulated in Artemia cysts in which mitosis was arrested. Knockdown of Ar-Rsk2 resulted in decreased levels of cyclin D3 and phosphorylated histone H3, and the production of pseudo-diapause cysts. This indicates that Ar-Rsk2 regulates mitotic arrest. PLK and ERK RNAi showed that Ar-Rsk2, but not Ar-Rsk1, could be activated by PLK-ERK in Artemia. This is the first study to report that RSK isoforms with and without an ERK-docking motif regulate mitosis and meiosis, respectively. This study provides insight into the relationship between the structures and functions of RSK isoforms.
Highlights
Ribosomal S6 kinase (RSK) plays important roles in meiosis and mitosis
This isoform was compared with an ribosomal S6 kinase (RSK) isoform that we previously identified in Artemia, termed Ar-Rsk1
Mitosis eventually resumed following diapause termination, and embryos developed into nauplii and metanauplii. These results show that meiosis was arrested in late oogenesis, whereas mitosis was arrested in diapause and post-diapause embryos
Summary
Ribosomal S6 kinase (RSK) plays important roles in meiosis and mitosis. Results: Ar-Rsk promoted cdc phosphorylation and thereby meiotic arrest, whereas Ar-Rsk knockdown resulted in mitotic arrest. Knockdown of Ar-Rsk resulted in decreased levels of cyclin D3 and phosphorylated histone H3, and the production of pseudo-diapause cysts This indicates that Ar-Rsk regulates mitotic arrest. PLK and ERK RNAi showed that Ar-Rsk, but not Ar-Rsk, could be activated by PLK-ERK in Artemia This is the first study to report that RSK isoforms with and without an ERKdocking motif regulate mitosis and meiosis, respectively. Ar-Rsk, which lacks an ERK-docking motif, played an important role in regulating CSF and meiotic arrest. Ar-Rsk, which has an ERK-docking motif, functioned in the regulation of mitotic arrest This study provides an insight into the relationship between the structures and functions of RSK isoforms
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