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Profilin Regulates Apical actin polymerization to Control Polarized Pollen Tube Growth

Molecular Plant 2015年第12期8卷 1694-1709页

作者： Xiaonan Liu Xiaolu Qu Yuxiang Jiang Ming Chang Ruihui Zhang Youjun Wu Ying Fu Shanjin Huang State Key Laboratory of Plant Physiology and Biochemistry College of Biological Sciences China Agricultural University Beijing 100193 China Key Laboratory of Plant Molecular Physiology Institute of Botany Chinese Academy of Sciences Beijing 100093 China Center for Plant Biology School of Life Sciences Tsinghua University Beijing 100084 China Tsinghua-Peking Joint Center for Life Sciences Beijing 100084 China National Center for Plant Gene Research Beijing 100101 China present address: Department of Biological Sciences Dartmouth College Hanover NH 03755 USA

Pollen tube growth is an essential step during flowering plant reproduction, whose growth depends on a population of dynamic apical actin filaments. Apical actin filaments were thought to be involved in the regu- lation of vesicle fusion and targeting in the pollen tube. However, the molecular mechanisms that regulate the construction of apical actin structures in the pollen tube remain largely unclear. Here, we identify profilin as an important player in the regulation of actin polymerization at the apical membrane in the pollen tube. Downregulation of profilin decreased the amount of filamentous actin and induced disorganization of apical actin filaments, and reduced tip-directed vesicle transport and accumulation in the pollen tube. Direct visualization of actin dynamics revealed that the elongation of actin filaments originating at the apical membrane decreased in profilin mutant pollen tubes. Mutant profilin that is defective in binding poly-L-proline only partially rescues the actin polymerization defect in profilin mutant pollen tubes, although it fully rescues the actin turnover phenotype. We propose that profilin controls the construction of actin structures at the pollen tube tip, presumably by favoring formin-mediated actin polymerization at the apical membrane.

关键词： pollen tube actin actin polymerization profilin formin

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Hydrogen sulfide promotes endothelial cell actin polymerization and is crucial to VEGF-induced cytoskeleton rearrangement

Hydrogen sulfide promotes endothelial cell actin polymerizat...

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中国生理学会第23届全国会员代表大会暨生理学学术大会

作者： Wen-Jie CAI~1,Ming-Jie WANG~2,Yi-Chun ZHU~2 1 Department of Basic medicine,University of Shanghai for Science and Technology,Shanghai 200093,China 2 Department of Physiology and Pathophysiology,Fudan University Shanghai Medical College,Shanghai 200032,China

Introduction:Hydrogen sulfide(HS),the toxic gas,has been shown to play an important role in regulating physiological functions.Our previous study has shown that HS enhances angiogenesis in vitro and in vivo.But whether hydrogen sulfide influences cytoskeleton rearrangement so as to promote cell migration? And furthermore,does endogenous HS participate in the VEGF or bFGF effect on cytoskeleton? The answer is still unclear.Methods:Rhesus monkey choroid retinal endothelial cells(RF/6A) were used.Rhodamine phalloidin was used to stain the cellular F-actin to show actin polymerization.Cells were exposed to different concentrations of NaHS(1-200μmol/L) for 20 min.K channel blocker Glibenclamide(10μmol/L) or CSE inhibitor DL-propargylglycine (PAG,10 mmol/L) was given 1 h prior.Cultures were then washed and fixed for 20 min in PBS containing 40 g/L paraformaldehyde,permeabilized,and incubated with Rhodamine-conjugated phalloidin for 40 min.Following washing,cells were imaged with a Leica TCS SP2 confocal laser microscope.Scanning and transmission electron microscopy were done to observe the ultrastructural changes of the cell skeleton.Results: Relatively low concentrations of NaHS(1 and 10μmol/L) enhanced endothelial cell skeleton reorganization and stress fiber formation.actin microfilament became thickened,tense and distributed with parallel manner.Furthermore, we observed that Glibenclamide partially prevented endothelial cell actin polymerization induced by 10μmol/L NaHS,while the Glibenclamide alone has little effects.10μmol/L NaHS treatment can turn the RF/6A endothelial cells into elongated shape and increased pseudopodia formation.VEGF(20 ng/mL) and bFGF(10 ng/mL) can both boost the stress fiber formation.PAG abolished VEGF induced but not bFGF induced cell skeleton reorganization. Conclusion:The present study provides the first evidence that HS enhance endothelial cell actin polymerization, partially via the mediation of K channel opening.Endogenous HS is crucial to VEGF-induced cytoskeleton rearrangement.

关键词： hydrogen sulfide endothelial cells migration actin polymerization

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