aflT, a MFS transporter-encoding gene located in the aflatoxin gene cluster, does not have a significant role in aflatoxin secretion

aflT, a MFS transporter-encoding gene located in the aflatoxin gene cluster, does not have a significant role in aflatoxin secretion
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DOI:
10.1016/j.fgb.2004.06.007
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发表时间:
2004-10-01
影响因子:
3
通讯作者:
Yu, JH
Yu, JH
中科院分区:
生物学3区
文献类型:
--
作者:
Chang, PK;Yu, JJ;Yu, JH

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aflT基因位于寄生曲霉黄曲霉毒素基因簇中的聚酮合酶基因pksA和编码cypA基因的P450之间。它是寄生曲霉 SRRC 2043 和 SU-1 基因组中的单拷贝基因,并且在黄曲霉分离株的基因组中也发现于相同的相对位置。预测的 AFLT 蛋白包含 14 个跨膜结构域,并且与属于主要促进子超家族的真菌转运蛋白具有不同程度的氨基酸同一性 (34-56%)。 A. parasiticus SU-1 中 aflT 的靶向删除产生了形态与 SU-1 相似的转化体。这些 aflT 缺失突变体产生和分泌的黄曲霉毒素与亲本菌株相当,尽管关键失去了 aflT 转录物的产生。实时RT-PCR分析表明,aflT的表达既不受黄曲霉毒素途径特异性激活子AFLR的控制,也不受共激活子AFLJ的控制,这与黄曲霉毒素生物合成基因pksA、nor1、ver1和omtA的调控不同。先前显示控制黄曲霉毒素生物合成和孢子形成的 FadA 依赖性 6 蛋白信号通路在 aflT 表达的调节中发挥作用。由爱思唯尔公司出版
The aflT gene resides between the polyketide synthase gene pksA and the P450 encoding cypA gene in the aflatoxin gene cluster of Aspergillus parasiticus. It is a single copy gene in the genome of A. parasiticus SRRC 2043 and SU-1 and was also found at the same relative position in the genome of Aspergillus flavus isolates. The predicted AFLT protein contained 14 transmembrane domains and had various degrees of the amino acid identity (34-56%) to fungal transporters belonging to the major facilitator superfamily. Targeted deletion of aflT in A. parasiticus SU-1 yielded transformants that were morphologically similar to SU-1. These aflT-deleted mutants produced and secreted aflatoxins comparable to the parental strain although key lost the production of the aflT transcript. Real-time RT-PCR analysis showed that the expression of aflT was controlled neither by the aflatoxin pathway-specific activator AFLR nor by the co-activator AFLJ, which differed from the regulation of the aflatoxin biosynthetic genes pksA, nor1, ver1, and omtA. The FadA-dependent 6-protein signaling pathway previously shown to govern aflatoxin biosynthesis and sporulation plays a role in the regulation of aflT expression. Published by Elsevier Inc.