傳媒

Figure 1. Overexpression of truncated ACBP4 variant promotes salt tolerance in soybean hairy roots. Soybean hairy roots overexpressing the native (bottom middle) and truncated (bottom right) forms of ACBP4 were more salt-sensitive and salt-tolerant than the vector-transformed control (bottom left), respectively. Under normal conditions, the hairy roots of all genotypes grew similarly (top panels). Scale bar = 1 cm.

圖1：截短ACBP4變體在大豆毛狀根的超表達提高耐鹽性。
原體 （上列中）和截短（下列右）ACBP4在大豆毛狀根超表達時，相比對照組（下列左）分別減少和提高耐鹽性。在正常條件下，所有基因型生長無異（上列）。比例尺 = 1公分。

Figure 2. Overexpression of truncated ACBP3 variants promotes salt tolerance in Arabidopsis. Transgenic Arabidopsis overexpressing the native Class II ACBPs and truncated ACBP3 variants were more salt-sensitive and salt-tolerant than the vector-transformed control, respectively. Scale bar = 1 cm.

圖2：截短ACBP3變體在轉基因擬南芥的超表達提高耐鹽性。截短 ACBP3變體的超表達株系比對照組更耐鹽。原體ACBP3及ACBP4的超表達株系則更敏感。比例尺 = 1公分。

Figure 3. Model for ACBP3/ACBP4-regulated generation of oxylipin signals during the salinity response. Under normal conditions, ACBP binding with acyl-CoAs (C18:2 and C18:3-CoAs) facilitates sequestration of an inactive lipoxygenase. High salinity triggers dissociation of this complex by a dual mechanism. First, phosphatidic acid signals compete with acyl-CoAs for ACBP binding. Second, pre-mRNAs are cut and rejoined in an unusual way (known as alternative splicing) to produce ACBP variants lacking the lipoxygenase-interacting domain. Thus, the lipoxygenase is activated to generate oxylipin signals for adaptive responses.

圖3：ACBP3及ACBP4調控高鹽環境下脂氧化物信號形成的示意圖。
在正常條件下，原體ACBP3/ACBP4與亞油/亞麻酰基輔酶Ａ及脂氧化酶結合，使其失去活性（左圖）。在高鹽逆境下，複合體在雙重機制調控下解離。其一，酰基輔酶Ａ在磷脂酸信號的競爭下與ACBP3/ACBP4解離（中圖）。其二，mRNA前體通過可變剪接，產生不能與脂氧化酶結合的截短ACBP3/ACBP4變體（右圖）。因此，被激活後的脂氧化酶產生脂氧化物信號，誘發適應性反應。