近日,，中科院植物所林金星研究組利用細(xì)胞生物學(xué)手段,，深入研究了裸子植物白皮松花粉管生長過程中,，一氧化氮（NO）對鈣離子,、微絲骨架,、囊泡轉(zhuǎn)運和細(xì)胞壁構(gòu)建的調(diào)節(jié)作用,。該成果發(fā)表在New Phytologist（2009，182(4): 851-862）雜志上,。
NO作為重要的信號分子,，參與調(diào)控花粉管極性生長,。通過應(yīng)用顯微注射、非損傷微測,、免疫熒光標(biāo)記等技術(shù),，研究人員發(fā)現(xiàn)：NO釋放劑促進(jìn)花粉萌發(fā)和花粉管伸長，并且具有濃度效應(yīng),，而抑制劑則抑制花粉萌發(fā)和花粉管生長,，具有濃度效應(yīng)，同時使花粉管頂端膨大,，喪失極性,；NO釋放劑促進(jìn)胞外Ca2+內(nèi)流，頂端Ca2+濃度梯度增加,，NO抑制劑抑制胞外Ca2+內(nèi)流,，頂端Ca2+濃度梯度降低；NO釋放劑還能夠促進(jìn)囊泡運輸,，使花粉管頂端的細(xì)微絲束解聚,，相反，NO抑制劑抑制囊泡運輸,，促進(jìn)花粉管中微絲聚合,，尤其在花粉管頂端形成粗的微絲束，并一直延伸到花粉管的最頂端,；此外,，NO使花粉管頂端酯化果膠增加而酸性果膠降低。
研究結(jié)果說明：在白皮松花粉管中,，NO促進(jìn)胞外Ca2+內(nèi)流,，從而維持胞內(nèi)Ca2+濃度梯度，進(jìn)而影響花粉管頂端微絲骨架的組裝,，促進(jìn)囊泡運輸,，使花粉管頂端酯化果膠累積，最終促進(jìn)花粉管的正常生長,。（生物谷Bioon.com）
生物谷推薦原始出處：
New Phytologist 31 Mar 2009 DOI:10.1111/j.1469-8137.2009.02820.x
Nitric oxide modulates the influx of extracellular Ca2+ and actin filament organization during cell wall construction in Pinus bungeana pollen tubes
Yuhua Wang 1,2,3 , Tong Chen 1 , Chunyang Zhang 1,2 , Huaiqing Hao 1 , Peng Liu 1,2 , Maozhong Zheng 1,2 , Franti?ek Balu?ka 4 , Jozef ?amaj 4,5,6 and Jinxing Lin 1
1 Key Laboratory of Photosynthesis and Molecular Environmental Physiology, Institute of Botany, Chinese Academy of Sciences, Beijing 100093, China ; 2 Graduate School of Chinese Academy of Sciences, Beijing 100049, China ; 3 The College of Horticulture, Nanjing Agricultural University, Nanjing 210095, China ; 4 Institute of Cellular and Molecular Botany, Rheinische Friedrich-Wilhelms-University Bonn, Department of Plant Cell Biology, Kirschallee 1, D-53115 Bonn, Germany ; 5 Institute of Plant Genetics and Biotechnology, Slovak Academy of Sciences, Akademicka 2, SK-95007, Nitra, Slovak Republic ; 6 Palacky University Olomouc, Faculty of Natural Science, Olomouc 771 46, Czech Republic
Nitric oxide (NO) plays a key role in many physiological processes in plants, including pollen tube growth. Here, effects of NO on extracellular Ca2+ flux and microfilaments during cell wall construction in Pinus bungeana pollen tubes were investigated.
Extracellular Ca2+ influx, the intracellular Ca2+ gradient, patterns of actin organization, vesicle trafficking and cell wall deposition upon treatment with the NO donor S-nitroso-N-acetylpenicillamine (SNAP), the NO synthase (NOS) inhibitor Nω-nitro-L-arginine (L-NNA) or the NO scavenger 2-(4-carboxyphenyl)-4, 4, 5, 5-tetramethylimidazoline-1-oxyl-3-oxide (cPTIO) were analyzed.
SNAP enhanced pollen tube growth in a dose-dependent manner, while L-NNA and cPTIO inhibited NO production and arrested pollen tube growth. Noninvasive detection and microinjection of a Ca2+ indicator revealed that SNAP promoted extracellular Ca2+ influx and increased the steepness of the tip-focused Ca2+ gradient, while cPTIO and L-NNA had the opposite effect. Fluorescence labeling indicated that SNAP, cPTIO and L-NNA altered actin organization, which subsequently affected vesicle trafficking. Finally, the configuration and/or distribution of cell wall components such as pectins and callose were significantly altered in response to L-NNA. Fourier transform infrared (FTIR) microspectroscopy confirmed the changes in the chemical composition of walls.
Our results indicate that NO affects the configuration and distribution of cell wall components in pollen tubes by altering extracellular Ca2+ influx and F-actin organization.
