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A Study of the Mechanism for Pollen Tube Growth

Abstract

Through this PhD thesis work, the mechanism for pollen tube growth is studied using combined modeling and experimental approaches.

In chapter 1 of this thesis, we proposed mathematical models for ROP1 activity oscillation at apex of pollen tubes. Our combined theoretical and experimental studies suggested that ROP1 activity oscillation depends on downstream ROP1 signaling events, F-actin assembly and calcium accumulation, which positively and negatively feedback regulate ROP1 activity, respectively. Our findings suggested a key role for calcium in the negative feedback regulation of ROP1 activity.

In chapter 2 of this thesis, we proposed and experimentally validated a model coupling both active ROP1 polarity establishment and pollen tube morphogenesis. We revealed that exocytosis is the key process linking ROP1 GTPase polarity establishment, cell wall pectin distribution and polarized cell growth. Through exocytosis mediated positive feedback loop, RopGAP mediated global inhibition and lateral diffusion of ROP1 GTPase on plasma membrane, active ROP1 GTPases polarity can be established and maintained. Once maintained, active ROP1 controls cell wall mechanics via control of pectin exocytosis and thus determines the shape of pollen tubes. Experimentally, we also validated the model through both genetic (ren1-1 mutant) and chemical (Latrunculin B treatment) perturbation of pollen tube morphogenesis process.

In Chapter 3 of this thesis, we studied the mechanism of endocytosis in pollen tubes. We revealed that two interconvertible phosphoinositides, PI(4,5)P2 and PI4P, function in different steps of clathrin-dependent endocytosis in pollen tubes. Whereas accumulation of PI(4,5)P2 is required for the initial steps of membrane invagination, PI4P is required for the later steps of closing and/or fission of invaginated membrane. Given previous findings that both the accumulation and the hydrolysis of PI(4,5)P2 are required for clathrin-mediated endocytosis in yeast and animal cells, a balance between PI4P and PI(4,5)P2 may provide a common mechanism underlying clathrin-dependent endocytosis in various eukaryotic systems.

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