Low-light stress compromises photosynthetic and energy efficiency and leads to spikelet sterility; however, the effect of low-light stress on pollen tube elongation in the pistil remains poorly understood. The gene RGA1, which encodes a Gα-subunit of the heterotrimeric G-protein, enhanced low-light tolerance at anthesis by preventing the cessation of pollen tube elongation in the pistil of rice plants. In this process, marked increases in the activities of acid invertase (INV), sucrose synthase (SUS) and mitochondrial respiratory electron transport chain complexes, as well as the relative expression levels of SUTs (sucrose transporter), SWEETs (sugars will eventually be exported transporters), SUSs, INVs, CINs (cell-wall INV 1), SnRK1A (sucrose-nonfermenting 1-related kinase 1) and SnRK1B, were observed in OE-1 plants. Accordingly, notable increases in contents of ATP and ATPase were presented in OE-1 plants under low-light conditions, while they were decreased in d1 plants. Importantly, INV and ATPase activators (sucrose and Na2SO3, respectively) increased spikelet fertility by improving the energy status in the pistil under low-light conditions, and the ATPase inhibitor Na2VO4 induced spikelet sterility and decreased ATPase activity. These results suggest that RGA1 could alleviate the low-light stress-induced impairment of pollen tube elongation to increase spikelet fertility by promoting sucrose unloading in the pistil and improving the metabolism and allocation of energy.
充足的光照是水稻產(chǎn)量、品質(zhì)形成的重要保障。由于地理位置的原因，一些地區(qū)寡照天氣時(shí)常發(fā)生，且隨著氣候惡化，長期陰雨寡照天氣逐漸出現(xiàn)在其它區(qū)域；此外，大氣污染引起的全球暗化現(xiàn)象（global dimming）已經(jīng)產(chǎn)生，水稻生產(chǎn)面臨光照不足的挑戰(zhàn)。開花期是產(chǎn)量形成的關(guān)鍵時(shí)期，此期遭遇弱光脅迫將誘導(dǎo)穎花敗育，致使產(chǎn)量大幅度下降。弱光引起的碳匱乏可能是花粉管伸長受阻的重要因素，但其潛在作用機(jī)制還有待闡明。
RGA1基因編碼異源三聚體G蛋白α亞基，在植物細(xì)胞的胞外信號轉(zhuǎn)導(dǎo)過程中起重要作用，已被發(fā)現(xiàn)與多種非生物脅迫有關(guān)，包括熱脅迫、干旱脅迫、高光脅迫和鹽脅迫等。然而，弱光下RGA1對水稻雌蕊組織能量代謝及花粉管伸長的影響仍不清楚。本文揭示了RGA1調(diào)控弱光下水稻雌蕊組織中花粉管伸長的生理機(jī)制。
弱光下，中花11背景的RGA1突變體（d1）結(jié)實(shí)率下降幅度顯著高于野生型（WT）及過表達(dá)植株（OE-1）；三個(gè)株系花粉粒育性、花藥開裂、柱頭花粉粒數(shù)及柱頭花粉萌發(fā)率差異較小，但弱光脅迫顯著抑制d1花粉管在雌蕊組織的伸長，表明花粉管伸長受阻是穎花敗育的主要原因。進(jìn)一步分析表明，雌蕊組織中ROS和Ca2+差異較小，但弱光下ATP及ATPase含量在d1植株中顯著下降，暗示能量缺乏及利用效率下降是弱光抑制d1花粉管伸長的重要因素。WT、d1和OE-1雌蕊組織碳水化合物含量、蔗糖轉(zhuǎn)化酶活性、蔗糖合酶活性，線粒體呼吸電子傳遞鏈復(fù)合體I、IV和V及AOX含量的差異性變化證實(shí)了以上結(jié)論。另外，弱光下外源蔗糖（INV促進(jìn)劑）和Na2SO3（ATPase促進(jìn)劑）添加可提高d1雌蕊組織INV、SUS、ATPase活性、ATP含量和結(jié)實(shí)率。綜上所述，該研究表明RGA1通過促進(jìn)同化物轉(zhuǎn)運(yùn)，增強(qiáng)和優(yōu)化能量產(chǎn)生、分配、利用效率，為弱光下花粉管在雌蕊組織的伸長提供了充足的能量，提高了水稻弱光耐受性。