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. 2009 Jun 16;60(12):3477–3489. doi: 10.1093/jxb/erp183

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© 2009 The Author(s).

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

This paper is available online free of all access charges (see http://jxb.oxfordjournals.org/open_access.html for further details)

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Fig. 6. — Proposed model of the relationship between the PI signalling system and formation of cell polarity in monospores. PtdIns(4)P produced by PI4K from PtdIns is phosphorylated by PIPK to generate PtdIns(4,5)P₂. PtdIns(4,5)P₂ can be hydrolysed by PLC to generate the second messengers IP3 and DG. IP3 then binds IP3R, which results in the release of Ca²⁺ from the cytoplasm. The inhibition of PLC, DGK, and IP3R in addition to Ca²⁺ influx prevents the establishment of cell polarity. The catalysis of PLC and PI3K depends on Ca²⁺ influx, which is triggered by light irradiation. DG is converted to PA by DGK. PA is also produced from PC by PLD. PA activates PIPK to produce PtdIns(4,5)P₂ as a precursor of the substrate of PLC and PtdIns(4,5)P₂ activates PLD which hydrolyses PC to produce PA. According to the function of PLD, the positive regulatory circuit indicated by the box drawn with a dashed line is proposed for the maintenance of cell polarity. Pharmacological reagents and their actions are indicated by red characters and bars.