Abstract
Fission yeast undergoes growth polarity transition from monopolar to bipolar during G2 phase, designated NETO (New End Take Off). It is known that NETO onset involves two prerequisites, the completion of DNA replication and attainment of a certain cell size. However, the molecular mechanism remains unexplored. Here, we show that casein kinase 1γ, Cki3 is a critical determinant of NETO onset. Not only did cki3∆ cells undergo NETO during G1‐ or S‐phase, but they also displayed premature NETO under unperturbed conditions with a smaller cell size, leading to cell integrity defects. Cki3 interacted with the polarity factor Tea1, of which phosphorylation was dependent on Cki3 kinase activity. GFP nanotrap of Tea1 by Cki3 led to Tea1 hyperphosphorylation with monopolar growth, whereas the same entrapment by kinase‐dead Cki3 resulted in converse bipolar growth. Intriguingly, the Tea1 interactor Tea4 was dissociated from Tea1 by Cki3 entrapment. Mass spectrometry identified four phosphoserine residues within Tea1 that were hypophosphorylated in cki3∆ cells. Phosphomimetic Tea1 mutants showed compromised binding to Tea4 and NETO defects, indicating that these serine residues are critical for protein–protein interaction and NETO onset. Our findings provide significant insight into the mechanism by which cell polarization is regulated in a spatiotemporal manner.
Highlights
Cell polarization is of fundamental importance for many biological processes
We previously showed that fission yeast CK1c, known as Cki3, is localized to the plasma membrane and that Cki3 kinase activity is required for the delay in NETO onset downstream of Cds1/CHK2 and calcineurin when S-phase is blocked (Kume et al 2011; Koyano et al 2015)
We propose that Tea1 phosphorylation through Cki3 at the cell tip plays an inhibitory role in NETO onset, which is attributable to compromised interaction with Tea4
Summary
Cell polarization is of fundamental importance for many biological processes. These include asymmetric. We previously showed that fission yeast CK1c, known as Cki, is localized to the plasma membrane and that Cki kinase activity is required for the delay in NETO onset downstream of Cds1/CHK2 and calcineurin when S-phase is blocked (Kume et al 2011; Koyano et al 2015). In this present study, we found that Cki played a critical role in the determination of the NETO timing during an unperturbed cell cycle. We discuss how NETO onset is regulated in a spatiotemporal manner through Cki and Tea
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