重金屬鎘(Cd)在植物體內的轉運途徑及其調控機制

王曉娟，王文斌，楊 龍，金 樑，宋 瑜，姜少俊，秦蘭蘭

1 上海科技館，上海自然博物館自然史研究中心，上海 200127 2 蘭州大學，草地農業科技學院，蘭州 730020 3 蘭州大學，資源環境學院，蘭州 730000

重金屬鎘(Cd)在植物體內的轉運途徑及其調控機制

王曉娟1,*，王文斌2，楊 龍2，金 樑1，宋 瑜2，姜少俊2，秦蘭蘭3

1 上海科技館，上海自然博物館自然史研究中心，上海 200127 2 蘭州大學，草地農業科技學院，蘭州 730020 3 蘭州大學，資源環境學院，蘭州 730000

重金屬鎘(Cd)的毒害效應與其由土壤向植物地上部分運輸有關，揭示Cd2+轉運途徑及其調控機制可為提高植物抗鎘性以及鎘污染的植物修復提供依據。對Cd2+在植物體內的轉運途徑，特別是限制Cd2+移動的細胞結構和分子調控機制研究進展進行了回顧。Cd2+通過共質體和質外體途徑穿過根部皮層進入木質部的過程中，大部分在皮層細胞間沉積，少部分抵達中柱后轉移到地上部分。為了免受Cd2+的危害，植物體產生了多種限制Cd2+吸收和轉移的生理生化機制：1)環繞在內皮層徑向壁和橫向壁上的凱氏帶阻止Cd2+以質外體途徑進入木質部；2)螯合劑與進入根的Cd2+螯合形成穩定化合物并區隔在液泡中；3)通過H+/Cd2+離子通道等將Cd2+逆向轉運出根部。植物共質體和質外體途徑轉運重金屬鎘的能力以及兩條途徑的串擾尚待進一步明晰和闡明。

重金屬；鎘；共質體途徑；質外體途徑；調控機制

鎘(Cd)是一種毒性很強的重金屬，對植物生長和發育而言屬于非必需元素，輕度脅迫導致植物葉片干枯萎黃，根莖縮短，側根數量減少，降低營養元素吸收，而重度脅迫則會減少葉綠素含量，擾亂水分平衡，抑制抗氧化酶活性，引起活性氧(reactive oxygen species，ROS)合成積累，降低細胞膜通透性，導致細胞損傷，進而顯著抑制植物生長[1-2]。當前，自然環境中植物地上部分的鎘含量呈現增加趨勢，既是環境中鎘污染程度增加所致，也是植物自身在鎘脅迫下進化的結果[3]。隨著對鎘污染環境下土著植物的不斷篩選，一些鎘的超累積植物不斷被發現[4]。

重金屬鎘發揮毒性的關鍵步驟是其被吸收進入根內并向植物地上部分運輸，該過程受到植物外部和內部條件的影響。其中，影響根吸收鎘的外部條件如土壤鎘濃度、有機物含量、pH值、氧化還原電位、溫度和其它元素濃度等研究進展已有評述[5]。由于植物地上部分對鎘毒害作用更加敏感，為了減少Cd2+向地上部分的轉移，植物體內部阻礙Cd2+進入木質部和韌皮部并限制其向上轉運的機制已經引起了人們的關注。研究發現，細胞內部的螯合劑可以將鎘螯合后隔離在液泡中，阻止Cd2+以共質體途徑(symplastic pathway)橫向運輸，減少抵達木質部和韌皮部Cd2+的數量，進而減弱重金屬鎘向地上部分運輸。在細胞外部，鎘沿著細胞壁中的空隙從表皮、皮層到內皮層，經質外體途徑(apoplastic pathway)進入木質部向上轉運至植物的枝葉中[6]。由于植物內皮層細胞壁中不透水的凱氏帶會阻止Cd2+的運輸，因此Cd2+進入內皮層后又轉為共質體途徑[7]。本文著重回顧了鎘轉運途徑及其調控機制研究進展，為植物抗鎘性機制和鎘污染防治提供理論依據。

1 植物體內Cd的吸收和轉運途徑

土壤中的鎘在轉移進入植物體內各組織器官后才會產生毒害效果，共質體途徑是指Cd2+從植物根毛細胞膜上的通道進入，再利用細胞與細胞間的胞間連絲，經由皮層、內皮層及周鞘進入根內導管細胞，而質外體途徑則是土壤中的Cd2+經由根吸收之后不進入細胞內，而是沿著細胞壁中的空隙從表皮、皮層到內皮層，進入木質部和韌皮部[6]。鎘通過以上兩種運輸途徑抵達維管束并向枝葉轉運，隨著植物的生長和新陳代謝，逐漸被稀釋或排出體外，進而減少對植物的危害。雖然植物地上部分的鎘含量會隨著土壤中鎘濃度的增加而增加，但達到一定程度后就不再升高,如龍葵(Solanumnigrum)和中國石竹(Dianthuschinensis)地上部分的鎘含量最高分別為1110mg/kg和414mg/kg[8]。由于鎘毒害嚴重威脅植物生長，導致其光合作用和蒸騰作用幾乎停止，進而影響離子轉運，因此，植物產生了多種限制Cd2+吸收和轉移的生理生化機制以利于植物生長發育。研究發現，植物根系中的Cd2+含量通常高于地上部分，且地上部分對鎘更加敏感，表明植物可能通過限制鎘進入根中具有傳導水分和養分功能的木質部和韌皮部，以減少Cd2+向地上部分的轉運[9]。

1.1 影響鎘在植物體內轉運的外部因素

重金屬鎘并非地殼中含量豐富的元素，通常在巖石中伴隨大量的鋅而形成，土壤中鎘含量的范圍在0.1—2 μg/g，大多低于1 μg/g[10]。Cd在土壤溶液中溶解后，以水合離子、復雜的有機或無機化合物的形態存在，鎘向植物體內遷移受到諸多因素的影響，如土壤pH值、有機質含量、土壤中存在的其它元素和氧化還原電位等，其中土壤pH值和有機質含量是影響Cd2+在土壤中被植物吸收的主要因素。一方面，酸堿環境能夠決定土壤顆粒表面電荷的正負性質和Cd2+的存在形態，對于pH值較高的堿性土壤，Cd2+的遷移能力較低[11]。另一方面，Cd2+容易和土壤有機質的功能團如羧基、烯醇羥基、醇羥基等形成有機鎘絡合物而降低活性[12]。研究發現，植物根系分泌的可溶性有機物質導致根際土壤中Cd2+進入根部表皮受阻[13]。與此同時，鐵、錳等金屬元素的氧化物對土壤中Cd2+也具有吸附作用，可使其失去遷移能力[14]。

1.2 Cd2+進入根表皮層的途徑

植物根部吸收土壤溶液中Cd2+和被土壤顆粒吸附的Cd2+的部位主要在根尖，其中，根毛區吸收離子最為活躍，占鎘吸收的絕大部分[18]。意大利五針松(Pinuspinea)和海岸松(Pinuspinaster)根際表面會附著大量Cd2+，但其根尖上發達的根冠具有篩選離子并阻止鎘侵入的功能[19]。對玉米(Zeamays)根中鎘的沉積格局觀察發現，在低鎘濃度下Cd2+主要累積在根的頂端或距根尖3 cm的區域[20]。

圖1 玉米根中Cd2+的質外體(紅色)和共質體(綠色)轉運途徑示意圖Fig.1 Diagram of apoplastic (red) and symplastic (green) pathways to transport Cd2+ in Zea maysA 長細胞；B 短細胞；C 中柱鞘；D 木質部薄壁細胞；E 管胞。①根具有成熟的外皮層：Cd2+以質外體途徑進入表皮細胞壁后，受到正常發育的外皮層凱氏帶的阻礙；②根缺少成熟的外皮層，但具有成熟的內皮層：Cd2+以質外體途徑進入表皮層，之后通過中央皮層細胞壁的傳遞到達內皮層，正常發育的內皮層凱氏帶會阻礙Cd2+在細胞壁中進一步的傳輸，內皮層不具有凱氏帶時Cd2+可以順利通過內皮層，到達維管束；③中柱中的Cd2+以質外體途徑向中央皮層回流時會受到內皮層凱氏帶的阻礙；④根缺少成熟的外皮層：Cd2+通過共質體途徑能夠輕松穿過沒有凱氏帶的外皮層而進入維管束；⑤根具有成熟的外皮層，但外皮層細胞較短小：Cd2+首先進入外皮層和中央皮層細胞壁，進而穿過外皮層和中央皮層細胞膜進入表皮細胞的細胞質，細胞間通過胞間連絲傳遞Cd2+，使Cd2+進入維管束；⑥根具有成熟的外皮層，且外皮層細胞較長：Cd2+通過共質體途徑無法進入成熟的外皮層長細胞，不能到達維管束

1.3 Cd2+進入根木質部的途徑

本課題組對鎘脅迫條件下玉米幼苗的鎘沉積顯微觀察發現，Cd2+通過共質體和質外體兩種途徑進入根木質部，圖1示意了Cd2+在玉米根中的運輸途徑。Cd2+通過共質體途徑進入玉米的中柱，最后Cd2+又經過質外體擴散到導管或管胞。質外體途徑中的Cd2+在向中央皮層擴散時，受到外皮層凱氏帶的阻礙(圖1①)。當Cd2+到達發育正常的內皮層時，內皮層細胞壁中的凱氏帶一方面會阻止Cd2+的繼續擴散(圖1②)，另一方面，對于以共質體途徑進入木質部的Cd2+，凱氏帶也會阻止其通過質外體途徑返回中央皮層(圖1③)，使得木質部保持了較高的Cd2+濃度。共質體途徑中的Cd2+能夠順利穿過發育不正常缺失凱氏帶的外皮層細胞(圖1④)和具有正常凱氏帶外皮層的短細胞(圖1⑤)而進入細胞質，但不能穿過正常外皮層的長細胞(圖1⑥)。

鎘進入根細胞后通過共質體途徑到達中柱鞘，該轉運方式主要通過胞間連絲完成。有關Cd2+的共質體轉運形式尚不清楚，可能的形式有Cd2+和鎘螯合物兩種。重金屬鎘通過共質體途徑進入木質部主要利用重金屬酶P1B-ATP，如AtHMA2和AtHMA4編碼轉運蛋白，也有可能和YSL蛋白質結合進入木質部[16]。此外，擬南芥(Arabidopsisthaliana)AtPDR8基因編碼的三磷酸腺苷(ATP，adenosine triphosphate)轉運體已經被證明能夠將Cd2+從根毛和表皮細胞的細胞膜上導出[21]。業已證明，外皮層作為環境變化的屏障控制著水和離子的吸收[22]。大多數被子植物的外皮層與內皮層同時發育，外皮層是阻礙Cd進入根內的初級屏障，外皮層的存在可有效降低Cd2+通過質外體途徑進入根中[23]。外部環境因素能夠改變外皮層的發育速度，研究發現Cd2+會刺激外皮層使其發育加快，從而減少根系對鎘的吸收量[24]。

1.4 Cd2+在植物體內的轉運與沉積

鎘脅迫下植物的耐受機理主要包括解毒和轉運體系，其中，對鎘的解毒涉及到抗氧化防衛機制、鎘的螯合隔離以及外排機制等[25-26]；對鎘的轉運過程包括：根際活化吸附、經質外體途徑和共質體途徑的短距離運輸、經木質部及韌皮部裝載的長距離運輸[24]。大多數植物根中Cd2+的濃度高于莖葉，受根際Cd2+濃度的影響，根中鎘含量可能達到地上部分的10倍[27]。研究發現，根內鎘含量受土壤Cd2+濃度、鎘的有效性和鎘脅迫持續時間等因素的影響[28]。根際Cd2+濃度較低時，吸收的Cd2+主要向地上部分轉運，隨著鎘濃度進一步升高，根內Cd2+濃度迅速增加直至與外部達到平衡[29]。

根中的鎘濃度從外皮層薄壁組織到外皮層逐漸降低，中柱鞘中Cd2+的累積量很少，推測是Cd2+向不斷生長的側根轉移所致[30-31]。在維管束中鎘主要累積在傳導養分和水分的部位及其鄰近的薄壁細胞，表明Cd2+在長途運輸中不斷沉積[32]。值得注意的是在內皮層與木質部之間的薄壁細胞，其鎘含量高于鄰近維管束的薄壁細胞，這種結構可能與內皮層的細胞通道有關，相比于內皮層的凱氏帶，鎘更容易透過內皮層的細胞膜[29]。研究發現，高濃度鎘脅迫條件下Cd2+大量集中在根的中柱鞘和維管束組織，對主根的生長和側根的分生具有明顯的抑制作用[33]。

對于大多數植物，根中質外體通道含鎘最多，主要位于表皮、細胞壁和皮層細胞上，而細胞內的Cd含量很少，主要集中在液泡和細胞核內，有時也出現在細胞質和葉綠體中[34-35]。鎘敏感的植物較耐鎘植物其細胞壁中的鎘含量低而液泡中鎘含量高[36]。研究發現，大麥(Hordeumvulgrar)根中36%的Cd2+存在于細胞壁中，51%的Cd2+存在于細胞質中，后者34%—50%的Cd2+以螯合肽復合物的形式存在[37]，然而，在重金屬超累積植物東南景天(Sedumalfredii)和遏藍菜(Thlaspicaerulescens)中，70%—90%的Cd2+集中在細胞壁/質外體通道而不是細胞質/液泡中[38]。

研究發現，植物受鎘脅迫后細胞壁的陽離子交換能力加強[39-40]，透射電子顯微觀察顯示棉花(Gossypiumhirsutum)和遏藍菜中鎘顆粒出現在外層根組織細胞壁和細胞膜之間，維管束中少有分布[41-42]。也有研究發現，鎘顆粒主要出現在內皮層與木質部之間的質外體通道[29]以及內皮層與中柱鞘細胞的中間殼層[43]。通常，液泡中鎘顆粒聚集并形成大的沉淀物，其數量和大小隨鎘濃度的增加而增加[33]，成熟的根內鎘沉積在分生組織或外皮層薄壁細胞液泡中[29]。內皮層細胞中鎘則被隔離在液泡中或其大顆粒沉淀分布在靠近細胞壁的細胞質中，而維管束的鎘沉積發生在內皮層和木質部之間的薄壁細胞[42]，沉積在篩管和韌皮部細胞中的鎘進一步證明了植物對鎘向地上部分轉運的限制[29]。

2 植物抗鎘性的解剖結構基礎

根部外皮層由分裂成多層細胞的表皮構成，剩余外圍組織稱為皮質，內皮層將皮質與中柱鞘隔開，中柱鞘決定性的控制著溶質向地上部分的轉運，而形成凱氏帶的木栓質是影響中柱鞘細胞壁滲透性的主要物質[29, 44]。木栓質是構成凱氏帶的基本材料，其在成熟的內皮層細胞壁上呈線狀橫向分布，這些物質占滿內皮層細胞間的空隙，在細胞壁之間緊密連接，和質膜共同構成了根的質外體屏障，阻止溶質通過質外體途徑進入木質部與韌皮部[45]。

2.1 Cd2+在植物根系內部轉運的屏障

凱氏帶的形成代表根內皮層細胞發育的最初階段，是非常關鍵的時期[46]。凱氏帶的存在使水分和離子不能以質外體途徑穿過內皮層，只能通過內皮層細胞具有選擇性的質膜以共質體途徑向木質部轉運。根部內皮層細胞壁表面片狀木栓質的沉積過程，是內皮層發育的第二階段[45]。該階段內皮層表現出對質外體轉運的屏障作用，根尖以后的成熟區域嚴格控制水和溶質以質外體通道向木質部的流動[47]。栓質化能夠增強細胞對鎘脅迫的耐性，木栓質是栓質化過程的產物，其在根細胞壁中的含量影響著水和離子的流動。研究發現，擬南芥突變體由于內皮層木栓質的數量增加，顯著降低了水分進入木質部的流通性和地上部分Ca2+、Mn2+、Zn2+的富集量[48]。但是，木栓質在根中的數量差異可能不是唯一影響水分和溶質通過質外體途徑向木質部轉移的因素，其化學性質和沉積的微觀位置尚需深入研究[49]。此外，植物的周皮組織能夠抑制水、離子、氣體和病原菌的活動，對Cd2+的轉運也具有限制作用[50]。

與許多植物鹽脅迫加速根內皮層和外皮層的發育相似[51]，在含重金屬的廢棄礦渣上培育的玉米受到脅迫誘導內皮層細胞壁大范圍增厚[52]。因此，根外皮層和內皮層扮演著屏障的角色，限制Cd2+以質外體途徑進入根部[6]。當植物受到重金屬鎘脅迫時，質外體屏障受到感應，會在距離根尖很近的部位形成凱氏帶。Vaculík 等[53]觀察在不含鎘和含鎘(5 μmol/L)的營養液中培養10d的玉米幼苗，發現對照組發育形成的木栓質遠離根尖，占總根長的10%，而鎘處理組木栓質靠近根尖，占總根長的45%，表明鎘的脅迫刺激增大了內皮層木栓質區域，促使木栓質化提前和內皮層成熟加快。進一步研究發現，鎘脅迫不僅會導致玉米根內皮層木栓質和木質素含量增加，還會改變其化學構成[54]。以上改變可能是植物為減少鎘通過質外體途徑進入木質部而做出的適應性反應。

2.2 Cd2+脅迫下植物根形態結構的抗逆變化

3 Cd2+在植物體內的轉運調控

研究發現，許多植物的耐受性與液泡富集鎘的能力相關，液泡能夠大量富集鎘，則植物對鎘的耐受性強，反之則弱[6]。目前，已鑒定克隆了H+/ Cd2+逆向轉運通道同源基因AtCAX2和AtCAX4[65]、重金屬轉運酶P1B同源基因AtHMA3和ABC轉運同源基因AtMRP3[18]。與此同時，研究還發現巨噬細胞蛋白(NRAMP，natural resistance-associated macrophage protein)可以從液泡向細胞質中轉移鎘，相同功能的轉運蛋白還包括同源基因AtNRAMP3和AtNRAMP4的蛋白質[66]。

許多植物感應到鎘的侵入后，會產生螯合肽合成酶以促進螯合肽的形成，這些螯合肽能夠捕獲Cd2+形成無毒螯合物，并將其隔離在液泡中[5]。目前，植物螯合肽對鎘的解毒作用已經得到證實，大多突變會增強植物螯合肽合成酶基因的表達，對鎘的耐受性強于野生型，但也有突變會導致植物螯合肽合成酶產生缺陷，解毒性能降低，弱于野生型[67]。然而，自然生態系統中許多植物對鎘的耐受性和植物螯合肽合成酶的含量并不成正比，表明植物的抗鎘性還存在其他機理[68]。研究發現，鎘脅迫誘導了小麥和水稻金屬硫蛋白基因的表達，增加了植物中金屬硫蛋白的含量，說明其對提高植物抗鎘性和緩解鎘毒害具有積極作用[65,69]。

發生在根部外皮層的一些突變也與鎘的轉運調控有關，如圖1中④、⑤所示，正常的外皮層細胞應由成熟的長細胞(圖1中途徑⑥中所示)構成，但發生突變后長細胞缺失凱氏帶或變短小均會喪失對Cd2+的抵抗能力[59]。在根部缺少凱氏帶的區域，Cd2+和鎘的螯合物可能會唯一取道細胞外基質，以質外體途徑進入木質部(如圖1中途徑②所示)[70]。研究發現，陽離子通過質外體途徑進入木質部的過程一般會受到根尖末端橫向傳輸的限制[71]。雖然共質體和質外體途徑對傳遞Cd進入木質部的相對能力大小尚不清楚，但質外體途徑隨著根際溶液中Cd2+濃度的升高而增加Cd的吸收量，與Zn和Na的吸收機制一致[72]。支持質外體途徑參與鎘轉運的觀點認為根尖是根系中鎘流通最活躍的區域，且鎘的累積量與其根尖數成正比[73]。相反的觀點認為質外體途徑對鎘的運輸影響不大，以遏藍菜為材料的研究發現，24 h內從根部吸收轉運至地上部分的Cd2+與質外體途徑中的水流量呈負相關關系[74]，這與其他植物中蒸騰作用與鎘吸收富集呈正相關的研究結論不一致[75]。第三種觀點認為以共質體途徑傳遞鎘進入木質部之前，Cd2+和其它陽離子的吸收存在競爭作用，遏藍菜對Cd和Zn在地上部分的富積能力相差很大，表明植物對金屬離子的轉運具有選擇性和專一性，表明共質體途徑轉運Cd2+與蛋白質誘導有關[74,76]。

4 展望

由于鎘的共質體與質外體途徑之間呈現緊密的聯系和錯綜復雜的關系，迄今為止，關于鎘誘導根中央部位組織和細胞發生改變的研究較少，今后應進一步關注Cd2+以共質體和質外體途徑進入木質部的轉運過程，探析細胞間隙在鎘轉運過程中的作用。與此同時，木質部擔負著調節Cd2+向莖葉轉運的重要作用，木質部在受到鎘脅迫時會產生一定的應激反應，目前有關鎘離子對木質部功能與形態的影響尚不清楚，通過研究這種應激反應的機制并促進反應發生，有可能為減少根中Cd2+向地上部分轉移提供依據[77-78]。

進一步豐富植物耐鎘突變體庫，嘗試定向誘導植物產生較強的外皮層和缺失功能的內皮層，并開展相應的細胞學、生理生化和分子調控機制研究，在抵御外部重金屬鎘侵襲的同時使根中Cd2+容易進入木質部而向地上部分轉運并收獲移除，將為改造植物重金屬超累積性能和實施重金屬植物修復提供新思路。

綜上所述，今后應進一步明晰植物共質體和質外體途徑轉運重金屬鎘的能力，深入探究鎘脅迫下植物形態結構響應及其與抗鎘性的關系，闡明共質體和質外體途徑的分子調控機制，以增強根部耐受重金屬脅迫并促進Cd2+向植物地上部分轉移為目的，培育適合我國生態環境治理的超富集植物，最終實現植物修復技術在鎘污染土壤上的應用。

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Transport pathways of cadmium (Cd) and its regulatory mechanisms in plant

WANG Xiaojuan1,*, WANG Wenbin2, YANG Long2, JIN Liang1, SONG Yu2, JIANG Shaojun2, QIN Lanlan3

1NaturalHistoryResearchCenter,ShanghaiNaturalHistoryMuseum,ShanghaiScience&TechnologyMuseum,Shanghai200127,China2SchoolofPastoralAgricultureScienceandTechnology,LanzhouUniversity,Lanzhou730020,China3SchoolofEarthandEnvironmentalScience,LanzhouUniversity,Lanzhou730000,China

Heavy metal (HM) toxicity is a worldwide concern because it damages plants by altering their major physiological and metabolic processes. The heavy metal cadmium (Cd) is a nonessential element, and is a valid inhibitor of plant growth. The toxic effect of cadmium is closely related to its transfer from the soil to the plant above ground parts. Understanding the transport pathway and regulatory mechanism of cadmium in plants may improve plant resistance to this heavy metal, in addition to providing a theoretical basis for the phytoremediation soils contaminated by cadmium. In this paper, we reviewed the transport pathways of Cd2+in plants and what limits its mobility based on the cytological structural and molecular regulation mechanism of plants. As the main organ for transporting water and nutrients to the plant body, the plant root is also the main organ that absorbs toxic metals, such as cadmium. During the process of Cd2+transfer from the root cortex to the xylem, most Cd2+is deposited between the cells of the root cortex, with some reaching stele, before being transferred to the plant organs, such as the leaves in the above ground part of the plant. The transport pathway of Cd2+through the root cortex is mainly apoplastic, with the cytoplasmic accumulation of Cd2+possibly causing apoplastic transport towards the vascular cylinder to decline. The transport pathway of Cd2+in the vascular cylinder is also mostly apoplastic, with cytoplasmic accumulation reducing Cd2+transfer to the xylem. Since the aboveground parts of plants are more susceptible to Cd2+poisoning, two cellular strategies to restrict the absorption and transfer of cadmium have evolved. First, the Casparian strip surrounding radial wall and the endodermis wall prevents Cd2+from entering the root xylem via the apoplastic pathway. In addition, the Casparian strip promotes Cd2+transport via the endodermis, leading to vacuolar isolation and cytoplasmic precipitation. Second, heavy metal detoxification occurs by chelating Cd2+to form stable compounds, which are then deposited inside the vacuole. Third, excess cadmium also activates oxidative stress defense mechanisms and the synthesis of heavy metal stress related proteins to minimize metal toxicity, which includes the use of metallothiones and ion channels, such as H+/Cd2+binding or sequestrating Cd2+into vacuoles. For systematic improvements in the phytoremediation of heavy metal pollution, a more comprehensive understanding of cellular mechanisms involved in Cd avoidance, uptake, transport, and accumulation is required. Furthermore, the excluder strategy by extensive sequestration and retranslocation of cadmium through symplastic and apoplastic pathways should be confirmed and explored in future studies.

heavy metal; cadmium; symplastic pathway; apoplastic pathway; regulatory mechanism

國家自然科學基金(31270558)

2014- 04- 17; < class="emphasis_bold">網絡出版日期:

日期:2015- 05- 19

10.5846/stxb201404170754

*通訊作者Corresponding author.E-mail:wangxj@sstm.org.cn

王曉娟，王文斌，楊龍，金樑，宋瑜，姜少俊，秦蘭蘭.重金屬鎘(Cd)在植物體內的轉運途徑及其調控機制.生態學報,2015,35(23):7921- 7929.

Wang X J, Wang W B, Yang L, Jin L, Song Y, Jiang S J, Qin L L.Transport pathways of cadmium (Cd) and its regulatory mechanisms in plant.Acta Ecologica Sinica,2015,35(23):7921- 7929.