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JXB:西北寒旱所、蘭大丨FADs在植物脅迫耐受中的功能(鈣信號)

發(fā)布時間:2024-05-01
作者:中科院西北生態(tài)環(huán)境資源研究所石玉蘭、蘭州大學(xué)生科院安黎哲
標(biāo)題:integrated regulation triggered by a cryophyte ω-3 desaturase gene confers multiple-stress tolerance in tobacco
主題:ω-3脂肪酸去飽和酶在植物脅迫耐受中的功能
期刊:journal of experimental botany
影響因子:5.354
檢測指標(biāo):ca2+
英文摘要
ω-3 fatty acid desaturases (fads) are thought to contribute to plant stress tolerance mainly through linolenic acid (c18:3)-induced membrane stabilization, but a comprehensive analysis of their roles in stress adaptation is lacking.
here, we isolated a microsomal ω-3 fad gene (cbfad3) from a cryophyte (chorispora bungeana) and elucidated its functions in stress tolerance. cbfad3, exhibiting a high identity to arabidopsis atfad3, was up-regulated by abiotic stresses. its functionality was verified by heterogonous expression in yeast. overexpression of cbfad3 in tobacco constitutively increased c18:3 in both leaves and roots, which maintained the membrane fluidity, and enhanced plant tolerance to cold, drought, and salt stresses.
notably, the constitutively increased c18:3 induced a sustained activation of plasma membrane ca2+-atpase, thereby, changing the stress induced ca2+ signaling. the reactive oxygen species (ros) scavenging system, which was positively correlated with the level of c18:3, was also activated in the transgenic lines.
microarray analysis showed that cbfad3-overexpressing plants increased the expression of stressresponsive genes, most of which are affected by c18:3, ca2+, or ros. together, cbfad3 confers tolerance to multiple stresses in tobacco through the c18:3-induced integrated regulation of membrane, ca2+, ros, and stress-responsive genes. this is in contrast with previous observations that simply attribute stress tolerance to membrane stabilization.
中文摘要(谷歌機翻)
ω-3脂肪酸去飽和酶(fads)被認(rèn)為主要通過亞麻酸(c18:3)誘導(dǎo)的膜穩(wěn)定作用促進(jìn)植物抗逆性,但缺乏對其在脅迫適應(yīng)中的作用的綜合分析。
在這里,我們從冷凍植物(chorispora bungeana)中分離出微粒體ω-3 fad基因(cbfad3),并闡明其在脅迫耐受中的功能。表現(xiàn)出與擬南芥atfad3高度同一性的cbfad3被非生物脅迫上調(diào)。其功能通過酵母中的異源表達(dá)來驗證。煙草中cbfad3的過量表達(dá)在葉和根中組成性地增加了c18:3,這保持了膜的流動性,并增強了植物對冷,干旱和鹽脅迫的耐受性。
值得注意的是,組成型增加的c18:3誘導(dǎo)質(zhì)膜ca2+-atpase的持續(xù)活化,從而改變應(yīng)激誘導(dǎo)的ca2+信號傳導(dǎo)。與c18:3水平正相關(guān)的活性氧(ros)清除系統(tǒng)也在轉(zhuǎn)基因系中被激活。
微陣列分析顯示過表達(dá)cbfad3的植物增加了應(yīng)激反應(yīng)基因的表達(dá),其中大多數(shù)受c18:3,ca2+或ros的影響。 cbfad3一起通過c18:3誘導(dǎo)的膜,ca2+,ros和應(yīng)激反應(yīng)基因的整合調(diào)節(jié)賦予對煙草中多種脅迫的耐受性。這與先前的觀察結(jié)果形成對比,之前的觀察結(jié)果僅僅將壓力耐受性歸因于膜穩(wěn)定。
ca2+ fluxes in root tips treated with 15% peg or 200 mm nacl (n=10 ten-day-old seedling roots).
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