Abstract

SummaryCoordination of endomembrane biogenesis with cell cycle progression is considered to be important in maintaining cell function during growth and development. We previously showed that the disruption of PHOSPHATIDIC ACID PHOSPHOHYDROLASE (PAH) activity in Arabidopsis thaliana stimulates biosynthesis of the major phospholipid phosphatidylcholine (PC) and causes expansion of the endoplasmic reticulum. Here we show that PC biosynthesis is repressed by disruption of the core cell cycle regulator CYCLIN‐DEPENDENT KINASE A;1 (CDKA;1) and that this repression is reliant on PAH. Furthermore, we show that cyclin‐dependent kinases (CDKs) phosphorylate PAH1 at serine 162, which reduces both its activity and membrane association. Expression of a CDK‐insensitive version of PAH1 with a serine 162 to alanine substitution represses PC biosynthesis and also reduces the rate of cell division in early leaf development. Together our findings reveal a physiologically important mechanism that couples the rate of phospholipid biosynthesis and endomembrane biogenesis to cell cycle progression in Arabidopsis.

Highlights

  • Plant growth and development are primarily driven by the production of new cells (Polyn et al, 2015)

  • To determine whether CYCLIN-DEPENDENT KINASE A;1 (CDKA);1 function effects the activity of PAH in A. thaliana we performed enzyme assays (Eastmond et al, 2010) on extracts from developing rosette leaves of wild type, cdka;1D and cdka;1DE (Figure 1)

  • To investigate whether CDKA;1 function effects phospholipid metabolism we measured the rate of PC biosynthesis in the leaves by monitoring the incorporation of [methyl-14C]choline into lipids (Eastmond et al, 2010)

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Summary

Introduction

Plant growth and development are primarily driven by the production of new cells (Polyn et al, 2015). Phospholipids are the main building blocks of the plant endomembrane system (Ohlrogge and Browse 1995) and their biosynthesis must occur in conjunction with cell cycle progression. Temporal changes in phospholipid metabolism over the course of the cell cycle have been well-documented in mammals, fungi, algae, dinoflagellates and bacteria (Jackowski, 1994; Saitoh et al, 1996; Janero and Barrnett, 1981; Kwok and Wong, 2005; Joseleau-Petit et al, 1984; Knacker et al, 1985). Similar changes must take place in plants but surprisingly they have yet to be described, possibly because of difficulties in generating highly synchronised plant cell cultures (Kwok and Wong, 2005). There is currently no mechanistic understanding of how phospholipid biosynthesis is coupled to the cell cycle in plants

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